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Digitized by VjOOQIC 




^i 7 ^ J' 


THE SESSION 1898-99. 



Digitized by VjOOQIC 

The present publication, being the Fiftieth Volume of Trans- 
actions, constitutes the Fifty-third published Annual Eeport of 
the Pathological Society's Proceedings. 

The Council think it right to repeat that the exhibitors are 
alone responsible for the descriptions given of the Specimens 
exhibited by them, the only change made in the Reports furnished 
by the authors being such verbal alterations as were absolutely 

20, Hakovbb Squabe, W. 
November, 1899. 

Digitized by 





List op Pbesidbktb of the Society .... it 

List OF Officebb aitd Membebb fob 1898-99 y 

Ajtitual Sepobt of the Council fob 1898-99 xxix 
LiBT of SpECiMEirs Exhibited dubino the Sesbiov 

1898-99 xxxiii 

LiBT OF Specimens Bepobtep on by the Committee 


List of Plates . xltii 

List of FieuBES in the Text xlv 

Diseases, etc., of the Nebtous System . . 1 
Diseases, etc., of the Obgans of Eespibation . . 30 
Diseases, etc., of the Obgans of Cibculation . 41 
Diseases, etc., of the Oboans of Digestion 61 
Diseases, etc., of the Q-enito-ubinaby Obgans . 179 
Diseases, etc., of Bone and of the Oboans of Loco- 
motion 185 

Diseases, etc., of the Ductless Glands 202 

Diseases, etc., of the Skin 220 

Mobbid Geowths 223 

Bactebiolooy and Pathological Chemistby 256 

Miscellaneous Communications 319 

Discussion on Pseudo-Tub ebculosis .... 331 

Index .365 

Digitized by 


f rtsiDtnts of l|t S^mi^. 





1852 C^SAR H. HAWKINS, F.R.S. 

1857 Sm THOMAS WATSON, Babt., M.D., P.R.S. 

1859 Sib WILLIAM PERQUSSON, Babt., P.R.S. 

1868 Sib PRESCOTT G. HEWETT, Babt., P.R.S. 

1867 Sib JOHN SIMON, K.C.B., D.C.L.. P.R.S. 

1869 Sib RICHARD QUAIN, Babt., M.D., LL.D., P.R.S. 

1878 Sib WILLIAM JENNER, Babt., M.D., G.C.B., D.C.L., P.R.S. 



1881 Sib SAMUEL WILKS, Babt., M.D.. P.R.S. 


1887 Sib JAMES PAGET, Babt.. D.C.L., LL.D., P.R.S. 







Digitized by 




"^at§0lagical S>otietg of |^onVon, 


Fob the Session ] 899-1900. 


















Sonorars SKXtimn 

M.D. I M.S. 


Digitized by 


llmbm of i\t glarbii (drototljs Committee, 



Digitized by 


*ii* Members are requested to inform the Senior Secretary of any corrections 
which may he necessary. 


^onoTarg Members. 

BoiroHABD, C, M.D., Professor of General Pathology, Paris. 

CHAirVKAU, A., M.D., Professor of Physiology at the Medical School of Lyons, 

EoOH, R., M.D.y Director of Institute for Infective Diseases, Berlin. 

The mght Honourable Lord Listbb, P.B.S., F.R.C.S., 12, Park crescent, Port- 
land place, W. 

Mbtohvikovf, £., M.D., Directenr de I'lnstitnt Pastenr, Paris. 

BUTDFLBISGH, Edouabd, M.D., Professor of Pathological Anatomy in the Uni- 
versity of Bonn. 

SlMOir, Sm JOHK, E.C.B., D.C.L., LL.D., F.B.S., 40, Kensington square, W. 

ViBOHOW, Rudolf, M.D., Professor of Pathological Anatomy in the University 
ef Berlin. 

Wblch, W. H., M.D., Professor of Pathology, Johns Hopkins University. 

ZiBOLEB, E., M.D. Professor of Pathological Anatomy, Freiburg. 


O.M. — Original Member. V.-P. — Vice-President. 

P. — President. S. — Secretary. 

T. — Treasurer. C. — Member of Council. 

M.G.C. — Member of the Morbid Growths Committee. 

The siimames of Members who have compounded for their subscriptions are 
printed in this type (TTPE). The surnames of Members who have paid the 
Composition Fee for the * Transactions ' are printed in this type (Type). 

Digitized by 




1801 Abbott^ Fbakcis Chablbs, M.S., 44, Welbeck street, W. 
1879 ABEBCBOMBIE, John, M.D.,28, Upper Wimpole street, W. (C. 1897^.) 
1885 Abbaham, Phikbas S., M.A., M.D., 2, Henrietta street, W. 

1806 Abbahams, Bbbtbah Louis, B.Sc, M.B., 14, Welbeck street, W. 
1868 AOLAim, Sir Hbnbt Wbntwobth, Bart., K.C.B., M.D., F.R.S., Broad 

street, Oxford. 
1888 AoLAND, Thbodobb Dtkb, M.D., 74, Brook street, W. (C. 1892-4.) 
1801 Adahi, J. Gbobob, M.A., Af.D., Montreal, Canada. 
1800 Adahs, Jahbs, M.D., 4, Cbiswick place, Eastbourne. 
O.M. ADAK8, WiLXJAH, 7, Londonn road, St. John's Wood, N.W. (C. 1851-4. 

V..P. 1867-0.) 
1848 AIKIH, Chablbb A., 12, Ladbroke terrace, W. (C. 1864-6.) 
1872 AilUK, Chablbs Edmund, 12, Ladbroke terrace, W. 

1807 Aloook, S. E., M.D., Portland House, Burslem. 

1888 ALLCHDT, Willuh Hbkbt, M.D., 5, Chandos street, W. 

1884 AKDBBSOir, Albxavdbb Riohabd, 6, East Circus street, Nottingham. 
1871 Akdbbsok, William, 5, Cavendish square, W. (C. 1888-90.) 

1807 AVDBBWBS, F. W., M.D., Highwood, Hampstead lane, Higbgate> N. 
1888 ASHBT, Hbitbt, M.D., 18, St. John street, Manchester. 

1868 Bagshawb, Fbbdbbigk, M.A., M.D., 85, Warrior square, St. Leonard's- 

1856 Balding, Dakibl Bablbt, Royston, Herts. 
1881 Ballakob, Chablbs A., M.S., 106, Harley street, W. (Hov. Sbcbbtabt). 

(C. 1890-2. S. 1800— .) 
1875 Babkbb. Abthub E. J., 87, Hurley street, W. (C. 1884-6. V.P. 1896-7.) 

1885 Bablino, Gilbbbt, M.B., 85, Edmund street, Birmingham. (C. 1894-7.) 
1874 BABLOW, Thomas, M.D.. B.S., 10, Wimpole street, W. (C. 1879-81. 

V.-P. 1894-6.) 
1890 Babbatt, John Oglbthobpb Wakbliv, M.D., West Biding Asylum, 

Wakefield, Torks. 
1877 Babbow, a. Botgb, 87, Wimpole street, W. 
1881 Babbs, Alvbbd Gbobob, M.D., 22, Park place, Leeds. 
1858 BASWXLL, Riohabd, 55, Wimpole street, W. (C. 1862-4. V.-P. 1880- 

1861 BA8TIAH, H. Chablton, M.A., M.D., F.R.S., 8a, Manchester square, W. 

(C. 1869-71. V.-P. 1885-7.) 
1877 Batbmav, Abthub W., B.A., Tenterfield, New South Wales. 

Digitized by 



1895 Battbk, Fbbdbriok E., M.D., 124, Harley street. W. 
1876 BATTESOir, John, Carnfortli, Chitwick lane» W. 
1882 Battlb, William HBUsy, 49, Hartey street, W. (C. 1898—.) 
1870 Baithlbb, Chbistian Q. H., M.D., University of Erlangen. 
1874 Beach, Flbtoheb, M.B., 64, Welbeck street, W., and Winchester Hoose, 

Kingston Hill, Surrey. 
1892 Bbadlbs, Cecil P., Colney Hatch Lnnatic Asylum, N. (C. 1898—.) 

1879 Bbalb, Edwin Cliftoed, M.B., 23, Upper Berkeley street, W. 

1852 BEALE, Lionel S., M.B., F.R.S., 61, Grosvenor street, W. (C. 1858>9. 

V..P. 1874-5.) 
1856 Bbalbt, Adah, M.D., M.A., Felsham Lodge, Hollington park, St. Leo- 

1897 Bbddabd, a. P., M.D., 44, Seymour street, W. 

1865 Bebbt, Waltbb, M.D., Bromley, Kent. 

1880 BEEYOB, Chaklbs Edwabd, M.D., 88, Harley street, W. (C. 1888-90.) 
1886 Bennett, Frrdebice Joseph, 17, George street, Hanover square, W. 

1877 Bennett, William Henry, 1, Chesterfield street, W. (C. 1891.3.) 
1889 Bentlet, Abthub, J. M., M.D., Mena House, Pyramids, Cairo, Egypt. 

1878 Bebnabd, Francis K., M.D., Prawls, Stone, near Tentcrdeu, Kent. 
1882 Berridqe, Williah Alered, Redhill, Surrey. 

1886 Berrt, Jahes, M.B., 21, Wimpole street, W. (C. 1895-7.) 

1891 Beyille, Fredbbice Wells, 19, New Cavendish street, W. 
1856 Biokeriteth, Edward R., 2, Rodney street, Liverpool. 

1882 Bindley, Philip Hbnry, M.B., Branksome road, St. Leonard's-on-Sea. 
1850 BIBKBTT, Edmund Lloyd, M.D., Westbonrne Rectory, Emsworth, 
Hampshire. (C. 1856-7.) 

1866 BissHOpp, James, Mount Pleasant, Tunbridge Wells. 
1889 Black, Robert, M.D., 14, Pavilion Parade, Brighton. 

1868 Blanchet, Jean B., M.D., M.S., Montreal, Quebec, Canada. 

1879 BoiLEAr, J. P. H., M.D., Brigade-Surgeon, Army. 

1876 Bond, Thomas, M.B., 7, The Sanctuary, Westminster, S.W. 

1869 Bourne, Walter, M.D. (Travelliug). 
1861 Bower, Richard Norris (Travelling). 

1881 Bowlby, Anthony A., 24, Manchester square, W. (M.G.C. 1884—. 

C. 1886-8. 1895-7. S. 1893-4. V.-P. 1898—.) 
1895 Box, Charlbs R., M.D., St. Thomas's HospitHl. S.E. 

1892 BOYCE, RUBBRT WiLLiAM, M.B., University College, Liverpool. 

1882 BoYD, Stanley, M.B., 134. Hurley street, W. (C. 1893-6. V.-P. 1897-9.) 
1889 Bradeord, John Rose, M.D., F.R.S., 8, Manchester square, W. (C* 


1880 Braxwbll, BYROif, M.D., 23, Drumshengh (rardens West, Edinburgh. 
1889 Brbdin, J. Noble, Linden Lodge, Potion, Beds. 

1877 Bridges, Robert, M.B., M.A., Manor House, Tattendon, Berks. 
1867 Bridgewatert Thohas, LL.D. Glas., M.B. Lond., Harrow-on-the-Hill, 

Digitized by 




1873 Bbiogs, Jacob Mtbrs, M.D.. Coeymans, New York, U.S.A. 
1868 Bbioht, Gboboe Chablbs, M.D., Cannes, Alpes Maritimes, France. 

1867 Bbisoob, John, 5, Broad street, Oxford. 

1885 Bbiscoe, John F., Westbrooke House, Alton, Hants. 

1860 BBOABBEITT, Sir William Hbnby, Bart., M.D., 84, Brook street, W. 
(C. 1871-8. V.P. 1882-4.) 

1886 Bbockatt, Andbrw Albxandeb, M.D., Hazeldean, Malvern. 
1852 BROBHUBST, Bbbnabd E., 21, Portland place, W. (C. 1862-4.) 

1884 Bkodib, Chables Gobdon, Fernhill, Wootton Bridge, Isle of Wight. 

1865 BBOWlf , Augustus, M.D., Felsberg, Wilton road, Shanklin, I.W. 
1871 Beown, Fbedbbick Gobdov, 17, Finsbury circus, E.G. 

1866 BBOWHE, Lennox, 15, Mansfield street, W. 

1877 Bbuob, J. Mitchell, M.D., 28, Harley street, W. 

1890 Bbunton, T. Laudeb, M.D., D.Sc, LL.D., F.R.S., 10, Stratford 
place, W. 

1898 Bbtant, John Hbnby, M.D., 8, St. Thomas's street, London bridge, 


1855 BBTAHT, Thomas, M.Ch., 66, Grosvenor street, W. (C. 1868-6. V.-P. 

1894 Buchanan, Gbobge Seaton, M.D., 9, Hammersmith terrace, W. 

1890 BUCKLAND, Fbancis O., M.A., M.B., CM., 10, Egerton place, S.W. 

1891 BUBGHABD, Fbbdbbic Fban^ois, M.D., M.S., 86, Harley street, W. 
1880 BUBTON, Samuel Hebbbbt, M.B., 50, St. Giles' street, Norwich. 

1878 BUTLIN, Henbt Tbentham, D.C.L., 82, Harley street, W. (M.G.C. 

1875-86. C. 1876-8, 1887-9. S. 1884-6. V.-P. 1891-2. P. 1895-7.) 
1888 BUXTON, Dudley W., M.D., 82, Mortimer street, W. 

1856 BUZZAED, Thomas. M.D., 74, Grosvenor street, W. (C. 1869-70. V.-P. 


1899 Caddy, Abnold, 2/2, Harington street, Calcutta. 

1885 Cahill, John, M.D., 12, Seville street, Lowndes square, S.W. 
1893 Caley, Hbnby Albbbt, M.D., 24, Upper Berkeley street, W. 

1897 Calvbbt, James, M.D., The Warden's House, St. Bartholomew's Hos- 
pital, E.C. 

1892 Campbell, Hbnby Johnstone, M.D., 36, Manningham lane, Bradford. 
1891 Cabless, Albbbt, M.S., 10, Welbeck street, W. 

1891 Cabb, John Waltbb, M.D., 19, Cavendish place, W. 

1876 Cabteb, Robert Bbudenell, 31, Hnrley street, W., and Kenilworth, 

Claphain common, S.W. 
1897 Cabwabdine, T., M.S., 16. Victoria square, Clifton, Bristol. 

1877 Casson, John Hobnsby, H.B.M. Legation, Teheran, Persia. 
1899 Cautley, Edmund, M.D., 15, Upper Brook street, W. 

1868 CAVAPT, John, M.D., 10, Fourth Avenue, Hove, Sussex. (C. 1881-8.) 
1864 Cay, Chables Vidleb, Deputy Surgeon General, 25, Newton place. 


Digitized by 




1868 Catlbt, William, M.D., 27, Wimpole street, W. (M.G.C. 1869-84. 

C. 1870-1. 1876-8. 8. 1872-4. V.-P. 1884-6. T. 1888-93.) 

1869 Chafvbbs, Edwabd, Eeighley, Torkshire. 

1884 Chapfbt, Watlakd Chablbs, M.D.« 18, Montpellier road, Brighton. 
1891 CflAPLiv, Abkolb, M.D., 41, Finsbnry square, E.G. 

1884 CHATA88B, Thomas Fbbdbbiok, M.D., CM., 22, Temple row, Bir- 

1879 Chbtvb, William Watson, M.B., CM., F.B.S. (Pbbsidbut), 75, 

Harley street, W. C. 1885-7. (M.G.C 1890-6. V.-P. 1892.8. 

P. 1899—.) 
1878 Chisholm, Edwin, M.D., Abergeldie, Ashfteld, near Sydney, New South 

Wales [care of Messrs. Dawson, 121, Cannon street, E.G.]. 
1866 CHUBCH, William Selbt, P.B.C.P., 130, Harley street. W. (M.G.C 

1869-74. C 1871-3. V.-P. 1894-6.) 
1868 CHURCHILL, Fbbdebick, M.D., 4, Cranley gardens, Queen's gate, 


1898 Chubton, Thomas, M.D., 85, Park square, Leeds. 

1861 CLAPTOir, Edwabd, M.D., Towercroft, 41, Eltham road, Lee, S.E. 

1872 Clabk, Andbbw, 71, Harley street, W. 

1886 Clabb, Fbanois William, M.B., Victoria, Hong Kong. 

1891 Clabbe, J. Jackson, M.B., 9, Old Cavendish street, W. 

1885 Clabsb. John Michbll, M.D.« 28, Pembroke road, Clifton, Bristol. 

1881 Clabkb, W. Bbucb, M.B., 51, Harley street, W. (C 1892-4.) 

1876 CLUTTOK, Hbnbt Hugh, M.A., 2, Portland place, W. (C 1884-6. 

M.G.C. 1889-94. V.-P. 1892-8.) 
1866 Coat«s, Chablbs, M.D., 10, Circus, Bath. 
1856 CoCKLB, John, M.A., M.D., The Lodge, West Molesey. 

1892 COLB, RoBBBT Hbnbt, M.D., 58. Upper Berkeley street, W. 

1886 CoLLiBB, William, M.D., High street, Oxford. 

1888 Collins, William Job, M.D., M.S., 1, Albert terrace. Regent's park, 

1878 CoLLTNS. R. T. Poole, 20, Lingfield road, Wimbledon. 
1888 CoLMAN, Waltbb Stacy, M.D., 22, Wimpole street. W. 

1882 CoLQUHOUN, Danibl, M.D., Dunedin, New Zealand. 
1896 Connbll, W. T., M.D., Kingston, Canada. 

1891 Cook, Hbbbbbt G. Gbaham, M.D., 22, Newport road, Cardiff. 

1858 COOKB, R. T. £. Babbington, 15, St. Nicholas cliff, Scarborough, Tork- 
1866 Coombs, Rowland Hill, M.D., Mill street, Bedford. 

1892 Coopbb, C. Dudlbt, 

1899 COBNBB, Habbt, M.D., Brook House, Southgate, N. 
1876 COTTLB, Wtndham, M.D., 89, Hertford street, W. 
1861 COUPEB, John, 80, Grosvenor street, W. (C 1870-2.) 

Digitized by 



1878 CouPLAVD, SiByxT, M.D. (Trbasfbbb), 16, Qaeen Anne street, W. 

(M.G.C. 1882-6. C. 1878-81. 1889-91. 8. 1886-8. V.-P. 1892-8. 

T. 1894—.) 
1897 Ceawfitkd, R. H. P.. M.D., 71, Harley street, W. 

1884 Cbichton, Gbobgb, M.D., 96, Earl's Court road, W. 

1878 Cbippo. William Habbison. 2, Stratford place, W. (C. 18836. V.-P. 

1877 CEOCKEE, Hbnbt Radclippb.M.D., 121, Harley street, W. (C. 1887-9. 

V.-P. 18979.) 
1856 Cboft, John, 6. Mansfield street, W. (C. 1870-2. V.-P. 1882-4.) 

1886 Cbookshank, Edoab, M.B., Saint Hill, East Grinstead, Sussex. (C. 

1875 Cbo38» Fbavcib Richabdsoit, 5, The Mall, Clifton, Bristol. 
1890 Cbowlb, Thohas H. Riceabd, 56, Harley street. Cavendish sqnare, W. 
1889 Cupp, Robbbt, M.B., 1, The Crescent, Scarbor.mgb. 

1885 CuLLiyowoBTH, Chablbs Jambs, M.D., 14, Manchester square, W. 
1871 Cumbbbbatch, A. Elbin, 80, Portland place, W. 

1878 CuBNOW, John, M.D., 9, Wimpole street, Cavendiih square, W. (C. 


1893 CuBTis, Hbnbt Jones, M.D., 60, Gower street, W.C. 

1884 Dakin, W. Radpobd, M.D., B.S., 18, Grosvenor street, Grosvenor square, 

1888 Daltok, Nobman. M.D., 4, Mansfield street, W. 
1873 Davidson, Albxandeb, M.D., 2, Gambier terrace, Livei pool. 
1869 DAVIES-COLLET, J. Neville C, M.C, 86, Harley street, W. (C. 

1880-2. V.-P. 1890-1.) 

1888 Davis, Edwin Habbt, West Hartlepool. 
1859 Davis, Fbanois William, R.N. 

1879 Davy, Hbnbt, M.D., 29, Southernhay, Exeter. 

1894 Dawson, Bebtband, M.D., 110, Harley street, W. 

1899 Dban, Gbobob, M.D., The Jenner Institute of Preventive Medicine, 
Grosvenor road, Chelsea Bridge, S.W. 

1889 Dean, Hbnbt Pbbct, M.B., M.S., 69, Harley street, W. 

1887 Dbl^pinb, Shbbidan, M.B., CM., Owens Colleg^e, Manchester. (C. 


1880 Dbnt, Clinton T., 61, Brook street, W. 

1871 Dickinson, Edwabd Habbiman, M.A., M.D., 51a, Rodney street, 

1858 DICKUrSOK, William Howship, M.D., 9, Chesterfield street, W. (C. 
1866-8. S. 1869-71. V.-P. 1872-4. P. 1889-90.) 

1890 DICKIV80K, William Lbb, M.D., 9, Chesterfield street, W. 

1872 DiVBB, Ebbnbzbb, M.D., 80, Devonshire street, W. 

1872 DoBAN, Alban Hbnbt Gbippiths, 9, Granville place, W. (C. 1882-4. 
V.-P. 1894-6.) 

Digitized by 




1866 Douglas- PowBLL, Sir Bichabp, Bart., M.D., 62, Wimpole street, W. 

(C. 1873-6, 1881-8. S. 1877-9. V.- P. 1887-8.) 
1898 DowsOK, Waltbb, M.D., 46, AUeyil road, West Dulwich. 
1877 Dbakb-Bbookmak. E. F., 14, Welbeck street, W. 
1880 Dbbsohfeld, Julius, M.D., 8, St. Peter's square Manchester. (C. 1896-9.) 

1896 Dbbw, Douglas, M.B., 58, Brook street, W. 

1879 Dbbwitt, F. O. Dawtbey, M.D., 2. Manchester sqnare, W. (C. 

1898 Dbysdale, JoHir Hannah, M.D.. 26, Welbeck street, W. 
1865 DUCKWORTH, Sir Dyce, M.D., LL.D., 11, Qrafton street, Bond street, 

W. (C.1877.) 
1847 DUDGEOH, Robbbt E., M.D., 63, Upper Berkeley street, W. 
1871 Dukes, Clbhbnt, M.D., B.S., Suunyside, Bngby. 
1877 Dunbab, J. J. MaoWhibtbb, M.D., Hedingham House, Clapham 

common, S.W. 
1889 Duncan, John, M.D., St. Petersburg. 
1884 Dunn. Louis At.bkbt, M.B.. M.S., The College, Guy's Hospital, S.E. 

1879 DuBHAM, Fbedebic, M.B., 82, Brook street, W. 

1893 EcoLES, William MoAdah, M.S., 124, Harley street, W. 
1892 Eddowbs, Alfbbd, M.D., 28, Wimpole streot, W. 

1880 EDMUNDS, Waltbb, M.C, 76, Lambeth Palace road, S.E. (C. 1892-4.) 

1882 Edwabds, F. Swinpobd, 55, Harley street, W. 
1889 Elam, William Hbnby, New Barnet, Herts. 

1883 Eldbb, Qbobgb,M.D., 17, Regent street, Nottingham. 

1867 Ellis, Jambs, M.D., Coburg street, Fratton, Portsmouth, and California. 
1863 Engelmann, Geobge Julius, M.D., A.M., 886, Beacon street, Boston, 

Mass., U.S.A. 
1876 Etans, Julian Augustus, A.M., M.D., 128, Finborough road, Redcliffe* 
square, S.W, 

1894 Etans, Willmott H., M.D., 18, Taviton street, Qordon square, W.C. 
1879 Eve, Fbedebic S., 125, Harley street, W. (M.O.C. 1884-94. C. 1886-7. 

V.-P. 1895-7.) 

1876 EwABT, Jambs Cossab, M.B., CM., F.R.S., School of Medicine, Edin- 


1881 EwABT, Sir Joseph, M.D., Bewcastle, Dyke road, Brighton. 

1877 BWART, William, M.D., 38, Curzon street, W. (C. 1889-91.) 
1859 Ewens, John, 17, Redland Grove, Bristol. 

1887 Etles, Chablbs Henbt, Gold Coast Colony. 

1897 Etbe, J. W. H., M.D., 14, Trinity square, S.E. 

1889 Faibbane, Fbbdebioe Royston, M.D., Hillside, Westcott, Dorking. 
1894 Fawcbtt, John, M.D., 24, St. Thomas's street, S.E. 

Digitized by 



1872 FsNir, Edwaed L., M.D., Orey Friare, Colchester. 
1883 Fenwick, E. Httsby, 14, Savile row, W. (C. 1894-7.) 
1872 Fbkwice, John C. J., M.D., Long Framlington, Morpeth. 
1868 FEVWICK Samuel, M.D.,29, Harley street, W. 
1892 Fenwick, W. Soltau, M.D., 8, Devonshire street, W, 
1886 FsEic, Chablbb, M.D., M^decin de Bic^tre; fioulevard St. Michel 37, 

1897 FiSHEB, Thbodobe, M.D., 25, Pemhroke rond, Clii'ton, Bristol. 

1882 Flbmikg, George, C.B., LL.D., Higher Leigh, Combe Murfcin, North 

1898 Flbtohbb, H. Moblbt, M.A., M.D., B.C., 98, Harley street, W. 
1872 Fobbbs, Danibl Maceay, 82, Oakfield road. West Croydon. 

1866 Foiter, Sir Balthazab Walteb, M.D., M.P., 80, Qrosvenor road, 

, Westminster. 

1872 Fothbbby, HByBY I., M.D., Woodthorpe Cote, Rcigate. 
1891 FoTTLBBTON, Alexandbb Qbakt Russell, Dunsdale, Mulgrave road, 

1880 FowLBB, Jambs Kingston, M.A., M.D., 86, Clarges street, W. (C. 


1878 Fox, Thomas Colcott, B.A., M.B., 14. Harley street, W. (C. 1892-4.) 
1858 Fbavcis, Chablbs Richabd,M.B., 15, Spencer pnrk. New Wandsworth, 

1896 Fbbybbbgbb, Ludwig, M.D., 41, Regent's park road, N.W. 

1891 Fbipp, Alpbbd Downing, M.S., 19, Portland place, W. 
1864 Fbodsdam, John Mill, M.D., Streatham, S.W. 

1894 Fubnivall, Pbbcy, 89, Welheck street, W. 

1898 Fyeeb, William Kington, M.B., 1, BouUcott street, Wellington, New 

1880 Oabbbtt, Hbnby Singbb, M.D., 8, Chiswick place, Easthourne. 

1858 Gairdner, Sir William Tbnnant, K.C.B.,M.D., LL.D.Edin., F.R.S., 

225, St. Vincent street, GUsgow. (V..P. 1891-2.) 
1890 Galloway, James, M.A., M.D.. 64, Harley street, W. (C. 1899—.) 
1870 Galton, John H., M.D., Sylvan road. Upper Norwood, S.E. 
1846 OARBOD, Sir Alfbbd Babing, M.D., F.R.S., 10, Harley street, W. (C. 

1851. v.. P. 1863-5.) 

1892 Gabbod, Abchibald Edwaed, M.D., 9, Chandos street. Cavendish 

square, W. (C. 1898—.) 

1879 Gabstang, Thomas Walteb Habbopp, Headiugley House, Knutsford, 

1872 Gabton, William, M.D., Inglewood, Aughton, near Ormskirk, Lanca- 

1880 Gibbbs, Hbkbagb, M.B., University of Michigan, Ann Arbor, Michigan, 

1868 GIBBON, Septimus, M.D., 89, Oxford terrace, Hyde park, W. 
1878 Gibbons, R. A., M.D., 29, Cadogan place, S.W. 

Digitized by VjOOQIC 



1893 GiBBS, Chablbs, 115, Harley street, W. 

1872 OiLBABT-SiciTB, Thomab, M.D., 68, Harley street, W. 
1876 GUL, John, M.D., 30, West mall, Clifton, Bristol. 

1881 Glynn, Thomas Robinson, M.D., 62, Rodney street, Liverpool. 

1898 GoADBT, Kbnnbth Wbldon, 6, Holly road, Cambridge park, Leyton- 

stone, Essex. 
1878 GoDLBB, RiCKMAN JoHN, M.B., M.S., 19, Wimpole street, W. (M.G.C. 

1875-84. C. 1877-80, 1891-2. 8.1887-9. V.- P. 1893-4.) 
1878 GoLDiNG-BiBD, CuTHBBBT H., M.B., B.S., 12, Qaeen Anne street, W. 

(C. 1886-7. V.-P. 1894-6.) 
1890 GooDALL, £. WiLBBBPOBCB, M.D., The Eastern Hospital, Homerton, 

1871 GooDHABT, Jambs Fbbdbbic, M.D., 25, Portland place, W. (M.G.C. 

1874-86. C. 1876-8, 1886-8. S. 1883-5. V.-P. 1892-3.) 

1894 GOSSAOB, Alfbbd Milnb, M.B., B.Ch., 54, Upper Berkeley street, W. 

1875 GoiTLD, Alfbbd Pbabob, M.S., 10, Qneen Anne street, W. (C. 1883-5. 

V..P. 1898—.) 
1870 GowBBS, Sir William, M.D., F.R.S., 50, Qneen Anne street, W. (C. 

1878-9. V.P. 1896-7.) 
1888 Gbant, J. DUNSAS, M.A., M.D., CM., 8, Upper Wimpole street, W. 
1867 Gbbbh, T. Hbnbt, M.D., 74, Wimpole street, W. (M.G.C. 1869-88. 

C. 1871-3,1878-9. 8.1875-6. V.-P. 1886-8.) 

1895 Gbbbv, Chablbs David, M.D., The Ferns, South street, Romford. 

1878 Gbbbnfibld, William Smith, M.D., B.S., 7, Heriot row, Edinburgh. 

(M.G.C. 1874-81. C. 1877-80. V.-P. 1898-4.) 

1886 Gbbtbs, Edwin Hyla, M.D., Rodney House, Suffolk road, Bourne- 


1897 Gbibbith, J., 16, Harley street, W. 

1887 Gbipviths, Josbph, M.D., CM., 63, Trumpington street, Cambridge. 

1876 Gbivfiths, Thomas D., M.D., Heame Lodge, Swansea. 

1887 Habbbshon, Samubl Hbbbbbt, M.D., 88, Harley street, W. 
1861 HACOV, £. Dbnnis, 269, Mare street. Hackney, N.E. (C. 1872.) 
1892 Hadlbt, Wilfbbd Jambs, M.D., 58, Harley street, W. 

1882 Haig, a., M.D., 7, Brook street, W. 

1899 Hall, A. J., M.B., 842, Glossop road, Sheffield. 

1894 Hallidib, Andbbw Hallidib Smith, M.B., 50, Noord street, Johannes- 
1886 Hamilton, Datid Jambs, M.B., 41, Queen's road, Aberdeen. 

1890 Hanovibld- JONBS, Montagu, M.D., 35, Cavendish square, W. 
1886 HAND70BD, Henby, M.D., 6, Regent street, Nottingham. 

1891 Hanein, E. H., Agra, India. 

1882 Habbinson, Albxandbb, M.D., County Lunatic Asylum, Lancaster. 

1898 Hablbt, Vaughan, M.D., 25, Harley street, W. 

1879 Habbis, Vincent Dobmbb, M.D., 22, Queen Anne street, W. 

Digitized by 




1891 Haslaic, William F., 54, Newball street, Birmiughatn. 

1870 Hawabd, Johk Wabeikotok, 67, Green street, Gro«venor square, W. 

(C. 1879-81. V..P. 1890-1.) 
1899 Hawkbs, Olaudb Soxebtillb, Rockbampton, Queensland, Australia. 
1886 Hawkins, Fbanoib Hbnbt, M.B., 73, London street, Reading. 
1890 Hawkins, Hbbbbbt Pbnnill, M.D., 66, Portland place, W. (C. 1898—.) 
1856 HEATH, Chbistophbb, 86, Cavendish square, W. (C. 1866-7. V.-P. 


1892 Hbaton, Gbobob, M.B., B.Ch., 33, Temple row, Birmingham. 

1881 Hbbb, Richabd G., M.A., M.D., 9, Suffolk street, S.W. (M.G.C. 

1891 -. C. 1891-8. 1898—. S. 1896-7.) 
1884i Hbbbbbt, Chablbs Alfebd, care of C. Baylor, 7, Water street, Boston, 


1878 Hbllibb, John B., M.D., 37, Park square, Leeds. 

1879 Hbndbbson, Gbobgb Coubtbnay, M.D., Kingston, Jamaica, West Indies. 
1869 Hbnslbt, Philip J., M.D., 4, Henrietta street, W. 

1884 Hbbbinohah, Wilmot Pabkeb, M.D., 13, Upper Wimpole street, W. 
(C. 1894-7.) 

1892 Hewlett, Richabd Tanneb, M.D., Jenner Institute of Preventive 

Medicine, Chelsea gardens, Grosvenor road, S.W. 
1897 HiCHENS, P. S., M.B., Bch., Hospital for Consumption. Brompton, W. 

1880 Hobson, John Mobbison, M.D., Glendalough, Morland road, Croydon. 
1854 HOLMES, TlicOTHT, 6, Sussex place, Hyde park, W. (C. 1862-8 S. 

1864-7. C. 1863. V.-P. 1869-71.) 
O.M. HcLTHOirsB, Cabsten, Helidon House, Shoeburyness, Essex. (C. 
1852-4. V.-P. 1874-6.) 

1878 Hood, Donald William Chablbs, M.D., 43, Green street. Park lane,W. 
1864 Hood, Whabton P., M.D., 11, Seymour street, W. 

1896 Hopkins, F. G., M.B., Now Museums, Cambridge. (C. 1899—.) 

1897 HOBNB, W. J., M.B., 27, New Cavendish street, Portland place, W. 

1879 HoBBOCKS, Petbb,M.D., 46, Brook street, W. 

1883 HOBSLSY, Viotob, M.B., B.S., F.R.S., 26, Cavendish square, W. (C. 

1896 Hoeton-Smitu, Pbboital,M.D., B.C., 15, Upper Brook street, W. 

1880 HOVELL, T. Mabe, 105, Hurley street, W. 

1893 HowABD, Robebt James Bliss, M.D., 81, Queen Anne street, W. 
1876 Howsb, Henby Gbbenway, M.S., 59, Brook street, W. (M.G.C. 1876- 

84. C. 1878-81.) 
1856 HUDSON, John, M.D., 11, Cork street, W. 
1874 Humphbbts, Henbt, M.D., St. Mnry Church road, Torquay. 

1897 Hunt, E. L., 18, Dorset square, W. 

1897 Hunt, G. B., M.D., 47, Albemarle crescent, Scarborough. 
1888 Hunteb, William, M.D., 103, Harley street, W. (C. 1897—.) 
1852 HUTCHINSON, Jonathan, F.R.S., 16, Cavendish square, W. (C. 1856-9. 
V.-P. 1872-3, 1881-3. P. 1879-80.) 

Digitized by 



1882 UuTOHIKBOH, JONATHAK, juu., 15, Ciivendish square, W. (C. 1889-91.) 
1884 Button, Henbt Richmond, M.B., 8a, St. John street, Manchester. 

1880 INGBAM, Ebvbst Fobtescub, Newcastle, Natal, S. Africa. 

1886 Jao^bok, Abthttb Moltnbvx, M.D., Kent County Asylum, Barming 

Heath, Maidstone. 
1865 Jaoksov, J. HuoHLiNOS, M.D., F.R.S., 8, Manchester square, W. (0. 

1872-3. V..P. 1888-9.) 
1886 Jackson, Philip J., 216, Great Dover street, S.E. 

1875 Jalland. William Hamsbton, St. Leonard's House, Museum street^ 


1897 James, G. T. B., Carlisle mansions, Victoria street, S.W. 
1888 James, Jambs Thomas, M.D., 80, Harley street, W. 

1868 Jardine, John Lee, Capel, near Dorking, Surrey. 

1897 JEKKEB, Louis, M.B., 4a, Bloomsbury square, W.C. 

1881 Jbnnings, William Osoab, M.D., Rue Marboeuf, Avenue des Champa 

Elys^es, Paris. 
1879 Jbssop, Chables Moobb, Clare Lodge, Redhill. 
1866 Jbssop, Thomas Richabd, 31, Park square, Leeds. 
1878 Johnson, Abthub Jukbs, Yorkville, Ontario, Canada. 

1876 Johnson, Chables Hbnbt, Winton House, Basingstoke, Hants. 

1888 Johnson, Raymond, M.B., B.S., 11, Wimpole street. Cavendish square, 

W. (C. 1896.9.) 
1854 Johnstone, Athol A. W., St. Moritz House, 61, Dyke road, Brighton. 
1858 JOHES, Stdnby, M.B., 18, Porthind place, W. (C. 1864-6. V.-P. 

1888 JoNBS, Taleoubd, M.B., Eastbourne. 

1862 JOHES, Thomas Ridgb, M.D., 4, Chesham place, S.W. (C. 1882-4.) 
1886 JULEB, Henbt Edwabd, 28, Cavendish square, W. 

1898 Keep, Abthub Cobbib, M.D., M.C., 7, Lower Seymour street, W. 

1867 Kelly, Chables, M.D., EUesmere, Gratwicke road. Worthing, Sussex. 
(M.G.C. 1872.4. C. 1874.) 

1897 Kelly, C. E. M., M.D., 9, Highbury grove, N. 

1879 Kestbvbn, William Henby, Hillwood, Waverley grove, Hendon, N.W 

1859 KiALLMABi, Henby Waltbb, 5, Pembridge gardens, W. (C. 1875-6.) 

1882 Kn>D, Pbboy, M.D., 60, Brook street, W. (C. 1889-91.) 

1867 King, Epwin Holbobow, 30, Norfolk square, Hyde park, W. 

1871 King, Robebt, M.B., Boyfield House, Moulton, Spalding, Lincoln- 

1862 KIKGDOK, J. Abebnethy, Threadneedle street, E.C. 

1888 Kynsey. Sir WilliaU Raymond, K.C.M.G., Oriental Club, Hanover 
square, W. 

1878 Lancbbeaux, Etiennb, M.D., 44, Rue de la Bienfaisance, Paris. 


Digitized by 



1882 Lanb, Williah Abbuthnot, M.B., M.S., 21, Cavendish square, W. 

(C. 1891.3.) 
1869 Labcheb, O., M.D.Par., 97, Rue de Passy, Paris. [M. Kliensieck, 

Libraire, Rue de Lille 11, Paris, per Messrs. Longmans.] 
1884 Labdbb, Hbbbbbt, Whitechapel Infirmary, Baker's row^ N.E. 
1897 Latham, A. C, M.B., 44, Brook street, W. 

1873 Latham, Pbtbb Wallwobk, M.D., 17, Trumpington street, Cambridge. 

1876 Law, William Thomas, M.D., 5, Duchess street, Portland place, W. 
1853 Lawbenor, Hbnbt John Ht7Qhbb, Picton House, Llandowror, St. Clears 

(C. 1873-6.) 

1892 Lavtbbnob, Thomas William Pblham, M.B., 64, South hill park, 


1893 Lawbon, Abnold, M.D., 12, Harley street, W. 

1859 Lawbon, Gbobgb, 12, Harley street, W. (C. 1870-1. V.-P. 1884-5.) 
1879 Laycook, Gbobge Lockwood, M.B., Melbourne, Victoria, Australia. 

1891 Lazabus-Bablow, Waltbb Sydney, M.D., Cecil House, Cavendish 

road, Sutton, Surrey. 
1875 Lediabd, Henby Ambbosb, M.D., 35, Lowther street, Carlisle. (C. 

1879 Lbeoh, Daniel John, M.D., 96, Mosley street, Manchester. 

1877 LEES, David B., M.D., 22, Weymouth street, W. (C. 1890-2.) 

1867 Lees, Joseph, M.D., 21, Brixton road, S.W. 

1877 Lesson, John Rudd, M.D., CM., 6, Clifden road, Twickenham. 

1868 Legg, John Wickham, M.D. (Travelling.) (C. 1874-5.) 

1892 Leith, Robebt Fbaseb Caldie, M.B., CM., B.Sc. 

1893 Lendet, Robebt, 16, Rue du Contrat Social, Rouen, France. 

1861 Lichtenbebg, Qbobgb, M.D., 47, Finsbury square, E.C 
1897 Listbb, Thomas David, 95, Wimpole street, W. 

1895 Little, Ebnest Gbaham Gobdon, M.D., 61, Wimpole street, W. 
1889 Little, John Fletoheb, M.B., 82, Harley street, W. 

1862 LITTLE, Loiris S., Shanghai, China. 

1896 Littlbwood, Habby, 40, Park square, Leeds. 

1874 LrvEiNG, Edwabd, M.D., 52, Queen Anne street, W. 

1863 LIVEIHG, Robebt, M.D., 11, Manchester square, W. (C 1876.) 
1882 LooEWOOD, C B., 19, Upper Berkeley street, W. (C 1893-6.) 
1881 LiTBBOOK, MoNTAGir, M.D., 19, Grosvenor street, W. 

1897 Lucas, Albbbt, 9, Easy row, Birmingham. 

1873 Lucas, R. Clement, M.B., B.S., 50, Wimpole street, W. (C. 

1879 LuNN, John Reuben, St Marylebone Infirmary ; Rackham street. Lad- 
broke grove road, W. (C 1897—.) 

1887 Lyon, Thomas Gloybb, M.D., 8, Finsbury circus, E.C 

1871 MAC COBMAC, Sir William, Bart.. K.C.V.O., 13, Harley street, W. 
(C 1878-80.) 

Digitized byCjOOQlC 



1893 McFadteax, John, M.B., Royal Veterinftry College, Great College 

street, N.W. (C. 1899— .) 

1896 Macpadybk, Allan, M.D., B.Sc, Jenner Institute of Preventive Medi- 
cine, Chelsea bridge, S.SV. 

1882 Maokbnzib, Fbedbbio Mobell, 29, Hans place, S.W. 

1885 Mackenzie, Hectob William Qatin, M.A., M.D., 59, Welbeck street, 

W. (C. 1895-7.) 
1870 Mackenzie, John T., Bombay, India. 

1878 Mackenzie, Stephen, M.D., 18, Cavendish square, W. (C. 1888-90.) 

1879 Maclagan, Thomas John, M.D., 9, Cadogan place, S.W. 

1865 MacLaubin, Henbt Nobmand, M.D., 187, Macquarie street, Sydney, 
New South Wales. 

1896 McWbeney, Edmond Joseph, M.D., M.Ch., 84, St. Stephen's green, 


1886 Maouibe, Robebt, M.D., 4, Seymour street, W. 

1877 Makins, Geobge Henbt, 47, Charles street, Berkeley square, W. (C. 
1889-91. V..P. 1899— .) 

1887 Malcolm, John David, M.B., CM., 13, Portman street, W. 
1892 Mann, Habold Edwabd, Alderney. 

1890 Manson, Patbick, M.D., CM., 21, Queen Anne street, W. 
1876 Maples, Reginald, Eingsclere, near Newbury. 

1868 Mabsh, F. Howabd, 80, Bruton street, W. (C 1876-7.) (V.-P. 


1887 Mabtin, Sidney, M.D., B.S., P.R.S., 10, Mansfield street, W. (C. 


1889 Mason, Datid James, M.D., Rosemont, Maidenhead. 

1867 Mason, Philip Bbookbs, Burton-on-Trent. 

1898 Mastebman, Ebnest William Gubnet, 3, Newnham terrace, Cam- 

1892 Mabtess, John Alfbed, M.D., 15, Half Moon street^ Piccadilly, W. 

1884 MAT7DSLEY, Henbt Cabb, M.D., 11, Spring street, Melbourne, Victoria. 

1897 Maxwell, J. P., c/o E.P. Mission, Amoy, China. 
1862 MAT, Geobge, M.B., Reading. 

1888 Mat, William Page, M.D.,B.Sc., 49, Welbeck street, W., and Helouan, 

near Cairo, Egypt (November to April). 

1881 Maylabd, Alpbbd Ebnest, M.B., 4, Berkeley terrace, Glasgow. 

1874 Mebbdith, William Applbton, CM., 21, Manchester square, W. 

1894 MiCHELS, Ebnbt, M.D., 6, West street, Finsbury circus, E.C 

1882 MOKET, AVGBL, M.D., Hunter street, Sydney, New South Wales. 

1879 MoOBE, NOBMAV, M.D., 94, Gloucester place, Portman square, W. (C. 
1885-7. M.G.C 1889— . V.-P. 1896-7.) 

1875 MoBGAN, John H., 68, Grosvenor street, W. (C 1886-8.) 

1874 MoBisoN, Alexandbb, M.D., CM., 14, Upper Berkeley street, W. 

1869 MoBBis, Henbt, M.A. (Tbustbb), 8, Cavendish square, W. (C 1877-9 

1884-6. S. 1881-8. V.-P. 18889.) 

Digitized by 




1879 M0BBI8, MALOOiic Albxakdbb, 8, Harley street, W. 

1894 MoBBiOB, Qbobge Gavin, M.D., Holy Trinity Vicarage, Weymouth. 
1891 MOBTOV, Chables A., 14, Vyvyau terrace, Clifton, Bristol. 
1876 MoBTON, John, M.B., Guildford. 

1884 MOTT, Pbedbbick Walkbb, M.D., F.R.S., 26, Nottingham place, W. 
(C. 1891-3. V.-P.1899— .) 

1893 MirifiCBBY, John Howabd, 10, Cavendish place, W. 

1876 MUNBO, William, M.D., CM., 13, King William street, K.C. 

1886 MUBBAY, HuBBBi MoNTAGVE, M.D., 26, Manchester square, W. 

(C. 1896-9.) 

1894 MiTBEAY, John, M.B., B.Ch., 110, Harley street, W. 

1887 Nason, Edwabd Noel, M.D., 80, Abbey street, Nuneaton. 
1873 Nettlbship, Edwabd, 6, Wimpole street, W. (C. 1882-4.) 
1876 Nbwby, Chablbb Hbnby, 16, Landport terrace, Southsea, Hants. 
1884 Newland-Pbdley, F., 32, Devonshire place, Portland place, W. 
1866 Nbwman, Williah, M.D., Stamford, Lincolnshire. 

1895 NiAB, J. Baldwin, M.D., 6, Rosary gardens, 8. Kensington, S.W. 
1868 Niohollb, Jakes, M.D., Trekenning House, St. Columb, Cornwall. 
1876 Nicholson, Fbank, M.D., 29, Albion street, Hull. 

1864 ISrOETOK, Abthub T., C.B., Ashampstead, Berks. (C. 1877-9.) 
1883 Nobyill, Fbbdebio Habvey, M.B., Dibrooghur, India. 
1866 NxTNK, Thomas William, 8, Stratford place, W. (C. 1864-6. V.-P. 

1880 O'CoNNOB, Bbbnabd, M.D., 26, Hamilton road, Ealing. 

1873 O'Fabbbll, Geobob Plunkbtt, M.D., 19, Fitzwilliam square, Dublin. 

1894 OOLE, Cybil, M.B., 96, Gloucester place, W. (C. 1899—.) 

1860 Ogle, John W., M.D., 96, Gloucester place, Portman square, W. (C. 

1856-6. S. 1867-60. C. I.S61-3. V.-P. 1866-8.) 
1876 Oliyeb, John Febens, M.D., 12, Old Elvet, Durham. 

1888 Opbnshaw, Thomas Hobbocks, M.S., 16, Wimpole street, W. 

1876 Obd, William Millbb, M.D., 37, Upper Brook street, W. (C. 1880-2. 

V.-P. 1893-4.) 
1892 Obd, William Wallis, M.D., The Hall, Salisbury. 
1879 Obmebod, J. A., M.D., 25, Upper Wimpole street. W. (C. 1887-9.) 
1876 OSBOEK, Samuel, 1a, Devonshire street, W., and Maisonnette, Datchet^ 


1881 Owen, Isambabd, M.D., 40, Curzon street, W. 

1866 OwLES, Jambs Allden, M.D., Hill View, Woking, Surrey. 

1870 Paget, Sir James, Bart., D.C.L., LL.D., F.R.S., 6, Park square We»t> 

Regent's park, N.W. (P. 1887-8.) 
1884 Paget, Stephen, 70, Harley street, W. (C. 1894-7.) 
1896 Paees, Walteb Chables, Guy's Hospital, S.£. 

Digitized by 




1897 PAB7ITT, Chablbs D., M.D., London, Canada. 

1898 Pabxbb, Abtuub Pbbot, M.B., B.Ch., Middlesex HoBpifcal, W. 

1872 Pabkbb, Robbbt William, 13, Welbeck street, W. (C. 1881-3. 

M.G.C. 188^94. V..P. 1897-9.) 
1874 Pabkbb, Rushtov, M.B., B.S., 59, Rodney street, Liverpool. 
1858 PABEniSOV, Gbobgb, Halsdown House, Exmontb, South Devon. 

1882 Pastbub, Williah, M.D., 4, Chandos street, W. (C. 1898-6.) 
1885 Paul, Fbakk Thomas, 88, Rodney street, Liverpool. 

1865 PAYY, Fbbdbbiok William, M.D., LL.D., F.R.S., 85, Grosvenor 

street, W. (0.1872-4. V.-P. 1891-2. P. 1898-4.) 
1868 Patkb, Joseph Fbavk, M.D. (Tbustbe), 78, Wimpole street, W. 

(M.G.C. 1872-85. C. 1878-5, 1883-5. S. 1880-2. V.-P. 1888-9. 

P. 1897-8.) 
1872 Pbabob, Joseph Chakikg, M.D., CM., Montague House, St. Lawrence* 

on-Sea, Kent. 
1879 Pbbl, Robbbt, 180, Collins street East, Melbourne, Victoria. 
1889 Penbbbthy, Johk, Royal Veterinary College, Camden Town, N.W, 

1887 Pbkbosb, Fbancis Gbobob, M.D., 84, Wimpolo street, W. 
1884 Pbppbb, Attgubtus Joseph, M.B., CM., 13, Wimpole street, W. 

1888 Pbbbt, EDwnr Coopbb, M.D., Superintendent's House, Guy's Hospital, 

1878 Philippb, Suthbbland Reeb, M.D., St. Ann's heatb, Virginia Water, 

1878 Phillips, John Waltbb, 30, Stanley street. West Melbourne, Victoria. 
1863 Pick, Thomas PiOKBBnrG, 18, Portmau street, W. (M.G.C. 1869-73. 

C. 1870-1. V.-P. 1885-7.) 
1896 PiOG, T. STBAyoBWAYS, New Museums, Cambridge. 
1893 PiKBEBTOK, Robbbt A., MJL., M.D., 15, South Norwood hill, S.E. 
1884 Pitt. Gbobgb Newton, M.D., 15, Portland place, W. (M.G.C 1889- 

97. C. 1890-2, 1896-9. S. 1894-6. V.-P. 1899—.) 
1876 Pitts, Bbbkabd. M.A.. M.C, 109, Harley street, W. (C 1888-90.) 

1883 Poland, John, 4, St. Thomas's street, Southwark, S.E. 

1882 POLLABD, BiLTON, M.B., B.S., 24, Harley street, W. (C 1895-7.) 
1850 Pollock, James Edwabd, M.D., 52, Upper Brook street, W. (C. 

1862-4. V.-P. 1879-81.) 
1870 PooBB, Gbobgb Vivian, M.D., 32, Wimpole street, W. (C. 1883-5.) 
1870 POTTXB, Henby Pebot, M.D., St. Mary Abbotts' Infirmary, Marloes road, 

Kensington, W. 

1884 POWEB, D'Abcy, M.A., M.B., 10a, Chandos street, W. (C. 1891-8, 

1899—. M.G.C. 1897— . 8.1897-9.) 
1865 PowEB, Henbt, 37a, Great Cumberland place, W. (C. 1876-7.) 

1887 Pbatt, William Stttton, M.D., Penrhos House, Rugby. 
1884 Pbicb, J. A. P., M.D., 124, Castle street, Reading. 

1856 PBIESTLET, Sir William Ovbbbnd, M.D., M.P., 17, Hertford 
street, W. 

1888 Pbimbobe, Albxandbb, M.B., CM.^ 196, Simcoe street, Toronto, Canada. 

Digitized byCjOOQlC 



1882 Peikolb, J. J., M.B., CM., 23, Lower Seymour street, W. 
1895 PiTEViB, William Pbiob,M.D.,2. Avenue place, Southampton. 
1865 Pye-Smith. Philip Hbney, M.D., P.R.S., 48, Brook street, W. (C. 
1874-7. V.-P. 1890-1.) 

1897 Raxein, Guthbib, M.D., 4, Chesbam street, S.W. 

1890 Bansom, William Bbamwbll, M.D., The Pavement, Nottingham. 

1891 Batoliffb, Joseph Riley, M.B., CM., Wake green, Moseley. 

1887 Bavek, Thomas Fbakcis, Broadstnirs, Kent. 

1870 Ray, Edwabd Reynolds, 67, Grosvenor street, W, 

1875 Rbid, Robebt William, M.D., CM., 8, Queen's gardens, Aberdeen. 

1881 Rbkneb, William, Wilberforce street. Free Town, Sierra Leone. 
1893 Rennie, Geobgb £dwabd, M.D., College street, Hyde park, Sydney, 

1895 Ritchie, Jambs, M.D., 28, Beaumont street, Oxford. 
1865 SobertS) Dayid Lloyd, M.D., 11, St. John's street, Manchester. 

1871 RoBEBTS,PBBDBBiOKTHOMAS,M.D.,102,Harley street, W. (C 1883-5.) 
1878 RoBEBTs, William Howland, M.D., Surgeon, Madras Army. 

1888 RoBBBTSON, RoBBBT, M.D., The Bungalow, Ventnor, Isle of Wight. 
1885 ROBINSOK, Abthub Hbkby, M.D., Mile End Infirmary, Bancroft road, 


1887 Robinson, Henby Betham, M.S., 1, Upper Wimpole street, W. (C. 


1882 Robinson, Tom, M.D., 9, Princes street. Cavendish square, W. 

1897 Rogee-Smith, Hugh, M.D., 1, College terrace, Fitzjobn's avenue, 

1888 RoLLESTON, Humphby Davy, M.A., M.D. (Hon. Secbetaby), 112, 

Harley street. (C 1894-7. M.G.C 1895— . S. 1898— .) 
1858 ROSE, Henby Coopbb, M.D., 16, Warwick road, Maida hill, N.W. (C 

1876 Rose, William, M.B., B.S., 17. Harley street, W. 

1875 Rosbiteb, Geoboe Fbedbbice, M.B., Cairo Lodge, Weston-super-Mare. 

1877 BOTH, Bbbnabd, 38, Harley street, W., and " Wayside," 1, Preston 

park avenue, Brighton. 
1888 Rovghton, Edmund Wilkinson, M.D., 38, Queen Anne street, W. 
1891 RouiLLABD, Lattbent Antoine John, M.B., Durban, Natal. 
1891 RuFPEB, Mabo Abmand, M.D., The Quarantine Board, Alexandria. 
1897 Rttndlb, H., 13, Clarance parade, Southsea. 
1895 RirssELL, Jambs Samuel Risien, M.D., 4, Queen Anne street, W. 
1891 Russell, William, M.D., 3, Walker street, Edinburgh. 

1854 Sandebson, Sir John Bubdon, Bart., M.D., D.C.L., F.R.S., 64, Banbury 

road, Oxford. (M.G.C. 1869-76. C 1864-7. V.-P. 1873-4.) 
1897 Santi. p. R. W. db, 42, Harley street, W. 

Digitized by 



1886 SAirirrBT, Robbbt, M.D., 88a, Edmund street, Birmingham. 

1871 Saxtitdebs, Ghablxs Edward, M.D., Sussex County Lunatic Asylum> 

Hay ward's Heath. ' 

1890 Saukdebs, Fbbdbbick William, M.B., B.C., Chieveley House, Newbury. 
1873 Satagx, Gxobge Hbnby, M.D., 3, Henrietta street. Cavendish square, 

W. (C. 1881-3.) 

1882 Savill, Thomas Dixoy, M.D., 60, Upper Berkeley street, W. 

1891 SoHOBSTXiK, GrsTAYE IsiDOBE, M.B., B.Ch., 11, Portland place, W. 
1877 Sbmon, Sir Felix, M.D., 39, Wimpole street, W. (C. 1885-7.) 

1894 Sbqubiba, Jambs Habby, M.D., 13, Welbeck street. Cavendish squai-e, W. 

1872 Sbboeant, £dwabd,D.F.H., Town Hall, Preston, Lancashire. 

1876 Shabbby, Sbymodb J., M.D., 22, Harley street. W. (M.G.C. 1834- 

95. C. 1884-6. V.-P. 1895-7.) 
1880 Shattock, Samuel G., 4, Crescent road. The Downs, Wimbledon, S.W 

(M.G.C. 1884—. C. 1885-7, 1893-6. S. 1890-2. V..P. ;i896-7.) 
1898 Shaw, Habold Batty, M.D., University College Hospital, Gower 

street, W.C. 
18^ Shaw, Laubiston Elgib, M.D., 10, St. Thomas's street, S.E. 

1886 SHEBRIHOTOK, Chables Scott, M.D., F.R.S., Holt Prof, of Physiol., 

University College, Liverpool. (C. 1894-7.) 
1856 SHILLITOE, Buxton, 2, Frederick's place, E.C. 

1875 SiDDALL, Joseph Boweb, M.D., CM., Conybeare, Northam, Bideford. 
1880 SiLCOCK, A. Quabby, M.D., B.S., 52, Harley street, W. (C. 1888*90.) 
1866 Sims, Fbanois Manlby Boldebo, 12, Hertford street, W. 

1892 Slateb, Chables, M.B., St. George's Hospital, S.W. 

1887 Smallpbioe, William Donald, 42, Queen Anne's gate, S.W. 

1875 8mo6, Alebbd Hutohinsok, The Grange, Hackbridge, Carshalton, 

1879 Smith, E. Noble, 24, Queen Anne street, W. 

1887 Smith, Fbbdbbick John, M.D., 138, Harley street, W. 
1875 Smith, Geobge John Malcolm, M.D., Hurstpierpoint, Sussex. 
1894 Smith, Guy Bellingham, M.B., B.S., 24, St. Thomas's street, S.E. 

1873 Smith, Riohabd T., M.D., 117, Haverstock hUl, N.W. 

1883 Smith, Robbbt Pebcy, M.D., 36, Queen Anne street, W. 

1869 Smith, Robebt Shingleton, M.D., Deepholra, Clifton Park, Bristol. 
1892 Smith, Solomon Chables, M.D., Four Oaks, Walton-ou-Thames, Surrey 
1866 Smith, Sir Thomas, Bart., 6, Stratford place, W. (C. 1867-9. V.-P* 

1866 Smith, William, Melbourne, Australia. 

1870 Smith, William Johnson, Seamen's Hospital, Greenwich, S.E. (C. 

1870 Snow, William Vicaby, M.D., Richmond Gardens, Bournemouth. 

1888 Solly, Ebnest, M.B., Strathlea, Harrogate, Yorks. 

1887 Spbnceb, Walteb Geobge, M.S., 35, Brook street, W. (M.G.C. 1894 — 

C. 1896-9.) 
1861 Squibe, Alexandeb Balmanno, M.B., 24, Weymouth street, W. 

Digitized byCjOOQlC 



1890 Stabb, Ewbn Cabthbw, 67, Queen Anne ftreet, W. 

1896 Stablikg^ Ebnist Hbnby, M.D., F.R.S., 8, Park sqnnre West, Regent's 
park, N.W. 

1896 Stbphbvb, J. W. W., M.D., Pathological Laboratory, Cambridge. 

1891 Stilbb, Habold Jallakp, M.B., CM., 6, Castle terrace, Edinburgh. 

1897 Still, G. F., M.D., 46, Gower street, W.C. 

1879 Stiblino, Edwabd Chablbb, C.M.G., M.D., F.B.S., Adelaide, South 
Australia [care of Messrs. Elder & Co., 7, St. Helen's place, E.C.]. 

1883 Stokbb, Gbobgb, 14, Hertford street^ W. 

1884 Stonham, Chablbb, 4, Harley street, W. (C. 1893-6.) 
1876 STirBOB,W. A.,M.D., 29, Boulevard Dubouchage, Nice. 

1871 SUTHEBLAHD, Hbkby, M.D., 21, New Cavendish street, W. 
1867 Swain, William Paul, 17, The Crescent, Plymouth. 

1881 STHoyPB, Chabtbbb Jambb, M.S., 58, Portland place, W. (M.G.C. 

1884-91. C. 1886-8. V.-P. 1899— .) 

1886 Taboett. Jambb Hbkby, M.B., M.S., 6, St. Thomas's street, S.K. 
(M.G.C. 1894—. C. 1894-6, 1897—. S. 1895-7.) 

1870 Tat, Wabbn, 4, Finsbury square, E.C. (C. 1881-2.) 

1871 TAYIOE, Fbbdbbiok, M.D., 20. Wimpole street, W. (M.G.C. 1879- 

89. C. 1879-81. V.-P. 1897-9.) 

1885 Tatlob, Hbnby H., 10, Brunswick place, Brighton. 

1892 Tatlob, Jambb, M.D., 49, Welbeck street, W. 

1879 Thin, Gbobgb, M.D., 63, Harley street, W. (C. 1889-90.) 

1852 THOMPSON, Sir Hbkbt, Bart.. 36, Wimpole street, W. (S. 1869-68. C. 

1866-7. V.-P. 1868-70.) 
1897 Thomson, H. Campbbll, M.D., 34, Queen Anne street, W. 

1891 Thomson, Hbnbt Albxib, M.D., 32, Rutland square, Edinburgh. 
1884 Thomson, John, M.D., CM., 14, Coates crescent, Edinburgh. 
1894 Thomson, StClaib, M.D., 28, Queen Anne street, W. 

1892 Thorbum, William. B.S., 2, St. Peter's square, and Rusholme Lodge, 

Rusholme, Manchester. 
1874 Thobnton, Jo^N Enowslbt, M.B., Hildersham Hall, Cambridge. 
1872 Thobnton, William Puoin, 86, St. George's place, Canterbury. 

1880 TiBABD, Nbbtob IsiDOBB, M.D., 74, Harley street, W. 
1884 TiVT, William Jamxs, 8, Lansdowne place, Clifton, Bristol. 

1897 TOOOOOD, P. Shbbman, M.D., The Infirmary, 282, High street, Lewis- 
bam, S.E. 

1882 Tooth, Howabd Hbnbt, M.D., 34, Harley street, W. (C. 1892-4. 

M.G.C. 1896—.) 

1886 TOTSUKA, Kankai, Tokio. 

1872 TOWKSEND, Thomas Sutton, 68, Queen's gate, S.W. 
1888 Tbevbltan, E. F., M.D., 40, Park square, Leeds. 

1881 Tbetes,Fbbdbbick, 6, Wimpole street, W. (C. 1887-90. V.-P. 1896-7.) 
1861 Tbotteb, John W., 4, St. Peter's terrace, York. (C. 1865-9.) 

Digitized byCjOOQlC 



1895 Tboutbbok, Hbnby, M.B., B.C., 148, Afhiey gardens, S.W. 
I860 TBUMAV, Edwin Thomas, 23, Old Barlington street, W. 

1888 'IVbby.AlfbbdHbbbebt, M.S., 25, Weymouth street, Portland place, W. 
1867 TuoKWELL, Hexbt Matthews, M.D., 64, High street, Oxford. 

1858 Tin>OB, John, Dorchester, Dorset. 

1875 TUBVEB, Fbanois Chablbwood, M.D., 16, Finsbnry squsre, E.C. (0. 

1884-6,1895-7. M.G.C. 1884-95. 8.1891-8. V.-P. 1898— .) 
1882 TuBNBB, Qbobgb Bobsbtsoi^, 41, Half Moon street, W. 

1863 TuBNBB, James Smith, 12, George street, Hanover square, W. 
1890 TiTBNEB, William Aldben, M.D., 13, Queen Anne street, W. 
1893 TuBNET, HOBAOB Gbobgb, M.D., M.Ch., 68, Portland place, W. 
1858 TUETLE, Fbbdbbioe, M.D., Kirkmead, Woodford, Essex. 

1880 Tyson, William Joseph, M.D., 10, Langhorne gardens, Folkestone. 

1867 Venning, Edgoombb, 30, Cadogan place, S.W. 

1889 VoELCKEB, Abthub Fbanois, M.D., B.S., 31, Harley street, W. (C. 


1867 WAGSTAFTE, William Wabwick, B.A., Purleigh, St. John's hill. Seven- 

oaks. (C. 1874, 1878-80. M.G.C. 1874-82. S. 1875-7.) 
1885 Waklby, Thomas, jnn., 5, Queen's gate, S.W. 

1893 Walkeb, Nobman Pubyis, M.D., 7, Manor place, Edinburgh. 

1881 Wallbb, Bbtan Chables, M.D., Masongill House, Cowan bridge, 


1890 Wallis, Fbbdbbioe Chables, M.B., B.C., 26, Welbeck street, W. (C. 


1888 Walsham, Hugh, M.A., M.D., B.C., 114, Harley street, W. 

1873 Walsham, William Johnson, M.B., CM., 77. Harley street, W. (C. 

1859 Waltebs, John, M.B., Reig^te, Surrey. 

1892 Wabd, Allan Ogieb, M.D.Edin., Lansdowne House, Tottenham. 
1892 Wabing, Holbubt Jacob, M.B., M.S., 9, Upper Wimpole street, W. 

1889 Washboitbn, John Wicheneobd, M.D., 6, Cavendish place, W. (C. 


1891 Watebhottse, Hebbebt Fubniyall, M.D., CM., 81, Wimpole street, 


1892 Weaveb, Fbedebick Poynton, M.D., Cedar Lawn, Hampstead Heath, 


1890 Webb, Chables Fbebe, M.D., New street House, Basingstoke. 

1894 WEBEB, Fbedebick Pabees, M.D., 19, Harley street, W. 

1858 WSBSE, Sir Hebmann, M.D., 10, Grosvenor street, W. (C. 1867-70. 
V.-P. 1878-80.) 

1864 Welch, Thomas Da vies, M.D. (Travelling). 

1894 Wells, Sydney Russell, M.D., 24, Somerset street, Portman square, 

Digitized by 



1892 Wesbbook, Pbank F., M.D.( Winnipeg). 

1877 Wbbt, Samuel, M.D., 15, Wimpole street, W. (C.1S84-6, 1891-3. S. 
1889-90. V..P. 1896-7.) 

1888 Wbthbbbd, Fbank J., M.D., 88, Harley street, W. 

1891 Wheaton, Samuel Walton, M.D., 76, The Chase, Clapham Common, 

1867 Whipham, Thomas Tilltee, M.D., 11, Grosvenor street, W. (C. 


1869 Whipple, John H. C, M.D., Royal Army Medical Corps. 
1877 White, Chables Haydon, 20, Shakespeare street, Nottingham. 
1894 White, Chables Powell, M.B., 130, Hyde park road, Leeds. 
1891 White, Gilbebt B. Mowbe, M.B., B.S., 112, Harley street, W. 
1881 White, Willlim Hale, M.D., 65, Harley street, W. (C. 1888-90.) 
1886 White, William Henby, M.D., 43, Weymouth street, W. 

. 1868 WUtehead, Waltbb, 17, Market street, Manchester. 
1897 Whitpield, Abthub, M.D., 12, Upper Berkeley street, Portmau 

square, W. 
1877 Whitmobe, William Tickle, 7, Arlington street, S.W. 

1870 Wice8teed,Fbanoi8 William, 2, Prince's mansions, Victoria street, S.W. 
1869 Wilkin, John F., M.D., M.C., Rose Ash House, South Molton, N. 


1871 Wilkinson, J. Sebastian, The Laurels, Oakengates, Salop. 

1855 WILKS, Sir Samuel, Bart., M.D., F.R.S. (Tbustee), 72, Grosvenor 

street. W. (C. 1857-60. V.-P. 1869-72, 1883-5. P. 1881-2.) 
1879 WiLLCOCKS, Fbedebick, M.D., 14, Mandeville place, W. 
1886 Willbtt, Edoab, M.B., 25, Welbeck street, W. (C. 1897—.) 
1869 WiLLUMS, Albebt, M.D. (Travelling). 

1858 Williftms, Chables, 48, Prince of Wales road, Norwich. 

1866 Williams, Chables Theodobb, M.D., 2, Upper Brook street, W. (C. 

1881 Williams, Dawson, M.D., B.S., 101, Harley street, W. (C.1898-6.) 

1872 Williams, Sir John, Bart., M.D., 63, Brook street, W. (C. 1878-80.) 
1881 Williams, W. Rogeb, Beaufort House, Clifton Down, Clifton. 

1 876 Williamson, James Mann, M.D., Ventnor, Isle of Wight. 
1863 Willis, Fbancis, M.D., Asheville, X. Carolina, U.S.A. 

1889 Wilson, Albebt, M.D., Leytonstone, Essex. 

1888 Wilson, Claude, M.D., CM., Church road, Tunhridge Wells. 

1859 Wilson, Edwabd Thomas, M.B., Montpelier terrace, Cheltenham. 
1891 Wilson, Theodobe Stagey, M.D., CM., 29, Temple row, Birmingham. 
1861 Windflor, Thomas, Medical Library, Boston, Mass., U.S. [care of B. F. 

Stevens, 4, Trafalgar square, W.]. 

1889 WiNOBAVE, V. Habold Wyatt, 11, Devonshire street, Portland 

place, W. 
1874 Wiseman, John Gbbates, Dearden street, Ossett, Yorkshire. 

Digitized byCjOOQlC 


1865 WiTHEBBT, William H., M.D., Pitt place, Coombe, Croydon. 

1883 WooDOOOE, JoHK RosTBOK, Abberley, near Stonrport, Worcestershire. 
1888 WooDHBAB, Gbbhav SniS, M.D., 6, Scrope terrace, Cambridge. 

(C. 1891-3. V..P.1898— . M.G.C. 1899— .) 
1879 WooDWABD, G. P. M., M.D., Deputy Surgeon General; Sydney, New 
South Wales. 

1884 WoBTS, Edwin, 6, Trinity street, Colchester. 

1869 Wtmak, William S., M.D., Red Brae, 18, Putney hill, S.W. 

1890 WnfNB, Edwabd T., M.B., Gladstone, Queensland. 

1884 Wtvtbb, Walteb Esbbx, M.D., 30, Upper Berkeley street, W. 

1872 Toiriro, Hbkby, M.B., Monte Video, South America. 

Digitized by VjOOQIC 

Digitized by 




TouB Council have to report the election of thirteen new 
members during the past session. There have only been five 
resignations, but the Society has lost by death ten members, 
including some of its most illustrious names. The actual number 
of members to-day is 679. The death roll this year includes Dr. 
Arkle, Mr. Blagden, Dr. Child, Prof. Coats, Mr. Thomas Cooke, 
Dr. C. J. Hare, Sir William Jenner, Prof. Kanthack, Dr. Port, 
and Prof. Eutherford. 

Sir William Jenner was President in 1873, and was an Honorary 
Member at the time of his death. Prof. Kanthack served on the 
Council of the Society from 1894 to 1897, and at the time of his 
death was a member of the Morbid G-rowths Committee. Prof. 
Coats was elected a member of the Society in 1885, but his official 
duties, and the distance of G-lasgow from London, had prevented 
him from accepting any office. Prof. Kutherford, the eminent 
Professor of the Institutes of Medicine at Edinbui^h, was elected 
a member in 1869, when he was Professor of Physiology at King's 
College, Loudon. The death of Sir William Jenner caused a 
vacancy in the list of honorary Fellows, which the Council filled 
by nominating the Eight Hon. the Lord Lister, P.B.S. 

The Morbid Q-rowtbs Conunittee co-opted Professor German 
Sims Woodhead, M.D., to the place of Professor Kanthack, a 
choice which was afterwards approved by the Council. 

In accordance with a previous decision of the Society, arrange- 
ments have been made to compile and issue an index to Vols. 

Digitized byCjOOQlC 


XXXVIII — L of the * Transactions.' A small committee was 
formed to consider the question of making an Index. After due 
deliberation the following report was drawn up, and was presented 
to the Council, who adopted it after considerable discussion. 

Tour Committee beg to report that they have held two meetings, 
and that they have decided unanimously to lay the following 
suggestions before the Council of the Pathological Society of 
London : 

(1) Although in 1887 the Council expressed a hope that it 
would be possible, in due course, to issue a G-eneral Index 
to the first fifty volumes of the * Transactions ' of the 
Society, your Committee find that the compilation of a 
new General Index would be a work of enormous labour, 
and that it would be too expensive for the funds of the 
Society. It seems probable that the printing and pro- 
duction of such a volume would cost no less than j£400, 
independently of any remuneration to the compiler or 

(2) The Committee recommend, therefore, that Indices be 
made (a) to all the plates and figures in the first fifty 
volumes of the Society's • Transactions ; ' (6) to the last 
thirteen volumes of the Society's ' Transactions,' viz. Vols. 
XXXVin — L. That these Indices be printed in a single 
volume, to be afterwards circulated amongst the members 
of the Society. 

(3) That Mr. Shattock be invited to undertake the work 
forthwith, that he receive an honorarium of Fifty 
Q-uineas, and that he be assisted by an Index Committee 
consisting of Dr. Payne, the President, Dr. Sidney 
Coupland, the Treasurer, Mr. D'Arcy Power and Dr. 
RoUeston, the two Secretaries, and Dr. Q-arrod, with 
power to add to their number. 

Signed on behalf of the Index Committee, 
November lUh, 1898. J. P. Payne, President. 

Mr. Shattock has undertaken to compile the Index, and he has 
already made considerable progress in his task. The Council 
reconunend that the expense of its production should be defrayed, 
if necessary, out of the capital funds of the Society. 

Digitized byCjOOQlC 


The interest of the Society's meetings during the session has 
been fully maintained, the average attendance of members on each 
evening being the same as last year, namely, thirty-three. The 
discussion on pseudo-tuberculosis resulted in the formation of a 
Committee of Members, who were "requested to consider the 
nomenclature of the condition." The report of the Committee is 
appended, and will be published in the forthcoming volume of the 
' Transactions.' 

The financial year began with a balance in hand of <£119 Ss, Id,, 
and closes with one of ^110 16«. Sd, Of this sum ^50 10«., 
representing the amount received from composition fees during the 
last four years, must be regarded as capital, and will be utilised 
to defray, in part, the cost of producing the General Index. It 
will be seen from the balance-sheet that on both sides of the 
account there has been a diminution in the amounts received 
and expended as compared with last year, the total income 
(JS450 3«. lOd,) being about ^30 and the total expenditure 
(^fi458 15«. Sd,) about ^23 less than for 1897-8. Compared with 
the average for the three preceding years — 1896-8 — the income 
derived from annual subscriptions and entrance fees — amounting 
to ^6370 13«.— shows a falling ofP of ^10. In respect to the 
main items of expenditure, that for the meetings — £144 15«. — 
is almost identical with the average of the three preceding years, 
whilst the cost of producing Vol. XLIX of the ' Transactions * — 
J6234 Us, 6d, — is about £30 below the average amount expended 
on Vols. XLVI— XLVIII. 

It is to be hoped that the funds of the Society will be increased 
by a greater influx of new members than has been the case 
hitherto, in order that the ordinary expenditure may be met 
without encroaching upon the capital fund, which now stands at 
^1114 Be, 2d. invested in Consols, and without starving the ' Trans- 
actions/ which form by far the most valuable memorial of the 
Society's work. 

J. F. Payne, 

May 16th, 1899. President, 

Digitized by 



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Digitized by 






1. A carse of embolism of both middle cerebral arteries, rheu- 

matic endocarditis, and carcinoma of the pancreas and 
liver Bj L. Pbetbebqeb, M.D. 1 

2. (1) Sarcoma of pineal body, with diffused melanotic 

sarcoma of the surface of cerebrum. (2) Tumour of 
pineal body in a boy [With Plate I] 

By Ctbil Oole, M.B. 4 

3. Tumour of the pineal body By T. W. P. Lawbence 12 

4. Pineal cyst By A. E. Gabbod, M.D. 14 

5. Cysts of the pineal body By A. E. Eussell, M.D. 15 

6. Notes of two cases of dilatation of the central cavity or 

ventricle of the pineal gland 

By A. W. Campbell, M.D. 15 

7. The pineal gland; its noimal structure; some general 

remarks on its pathology ; a case of syphiHtic enlarge- 
By John E. Lobd, M.B., introduced by Mr. Beadles 18 

8. Sarcomata involving the spinal cord of a child aged three 

years (Card specimen) By P. E. Batten, M.D. 21 

9. Further evidence on the pathology of diphtheritic para- 

lysis [With Plate II] 

By Pbedebick E. Batten, M.D. 22 
10. Neuroma of brachial plexus, with moUuscum fibrosum 

of skin By T. Cabwabdine, M.S. 27 


Digitized byCjOOQlC 




1. Case of ulcer of the trachea, involving the left recurrent 

laryngeal nerve, and perforating into the aorta (Card 
specimen) By Nobman Dalton, M.D. 30 

2. A case of pressure on the recurrent laryngeal nerves by 

calcareous glands, with anthracosis of the lungs (Card 
specimen) By Nobman Dalton, M.D. 31 

3. Transverse fracture of the cartilaginous portion of the 

trachea (Card specimen) 

By W. S. Lazabus-Bablow, M.D. 32 

4. Case of hypertrophy of the right lung with obliteration 

of the left By Nobman Dalton, M.D. 33 

5. Lung, showing uniformly distributed fibrosis (Card speci- 

men) By A. E. Gaebod, M.D. 36 

6. A case of sarcoma of left lung and mediastinum 

By Chables D. Gbeen, M.D., F.E.C.S. 37 


1. Dextrocardia; left superior vena cava; endocarditis 

(Card specimen) By Nobman Dalton, M.D. 41 

2. On dilatation of the right ventricle upwards and to the 

left By T. Stacy Wilson, M.D.Edin., M.R.C.P. 41 

3. Extreme dilatation of the left auricle without mitral 

stenosis (Card specimen) By H. Mobley Plbtghbb 48 

4. Spontaneous rupture of the heart (Card specimen) 

By Cecil P. Beadles 49 

5. Heart thrombus in a case of enteric fever ; embolism of 

the right common iliac artery ; incipient gangrene of 
the leg ; multiple infarcts in the spleen and kidneys 

By William Hunteb, M.D., P.R.C.P. 52 

6. Aneurysm of the splenic artery (Card specimen) 

By H. D. RoLLESTON, M.D. 55 

Digitized byCjOOQlC 



7. Aneurysm of splenic artery (Card specimen) 

By W. S. Lazaeus-Baelow, M.D. 57 

8. An apparent thickening of subcutaneous veins 

By P. Pakkes Wbbee, M.D., F.E.C.P. 57 

9. Tuberculosis of the inferior vena cava (Card specimen) 

By J. H. Detsdale, M.D. 60 


1. Actinomycosis of the tongue 

Exhibited by R. G. Hebb, M.D., for Mr. Ludfoed Coopee 61 

2. Congenital cyst of the base of the tongue 

By Raymond Johnson 62 

3. Epithelial pearls in the tonsil [With Plate III] 

By Hugh Walsham, M.A., M.D. 65 

4. A tumour arising in the region of the socia parotidis 

(Card specimen) By H. D. Rolleston, M.D. 66 

5. Adeno-lipoma of the submaxillary salivary gland 

By H. J. Waeino, M.S. 67 

6. Idiopathic hypertrophy of the oesophagus 

By H. D. Rolleston, M.D. 69 

7. Fusiform dilatation of the oesophagus 

By W. S. Lazaeus-Baelow, M.D. 71 

8. Myoma of the oesophagus (Card specimen) 

By H. D. Rolleston, M.A., M.D. 73 

9. Minute erosion (exulceratio simplex) of the gastric mucous 

membrane (Card specimen) 

By H. D. Rolleston, M.A., M.D. 73 

10. Gkkstric ulcer from a patient with granular kidneys (Card 

specimen) By H. D. Rolleston, M.D. 75 

11. Tubercular ulcer of the stomach in children 

By Geoeoe p. Still, M.D. 76 

12. A specimen of tubercular ulceration of the stomach from 

a child (Card specimen) By T. D. Listee, M.D. 83 

13. Myoma of the stomach (Card specimen) 

By Alexandes G. R. Foulbeton 85 

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14. Congenital hypertrophy of the pylorus 

By George F. Still, M.B. 86 

15. Congenital hypertrophy of the pylorus (Card specimen) 

By H. MoBLEY Fletcher, M.B. 98 

16. Carcinoma of the cardiac orifice of the stomach (Card 

specimen) By H. D. Eolleston, M.B. 99 

17. Carcinoma of the cardiac end of the stomach (Card 

specimen) By Aethxjb Voelckbb, M.B. 100 

18. Spheroidal-cell carcinoma of stomach involving the 

oesophagus (Card specimen) 

By W. S. Lazabus-Bablow, M.B. 101 

19. Case of colloid carcinoma of the stomach 

By E. G. Hebb, M.B. 102 

20. A case of gastrectomy for carcinoma of the stomach 

By Thomas F. Chavasse 105 

21. Carcinoma developing in the cicatrix of a gastric ulcer 

(Card specimen) 
By H. E. Belchee Hickman, M.B. (introduced by Br. 

Lazabus-Bablow) 109 

22. A specimen of duodenal ulcer from a case of melsena 

neonatorum (Card specimen) 

By T. B. LisTEB, M.B. Ill 

23. Healed perforation of duodenum after passage of gall- 

stones (Card specimen) By Cecil F. Beadles 113 

24. Three cases of sprue By J. H. Brysdale, M.B. 114 

25. Fatal summer diarrhoea with acute enteritis 

By F. W. Andbewes, M.B. 118 

26. Two unusual cases of intussusception 

By B'Abcy Powee 121 

27. Appendix vermiformis in which a pin was lodged (Card 

specimen) By H. A. Lediabb, M.B. 126 

28. Peculiar condition of the colon in pernicious anaemia 

By H. MoBLEY Fletcheb, M.B. 127 

29. A specimen of diffuse ulcerative colitis with secondary 

acute interstitial hepatitis (Card specimen) 

By T. B. LiSTEB, M.B. 130 

30. Villous papilloma of rectum (Card specimen) 

By T. Cabwabdine, M.S. 133 

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31. Enterolith from the rectum (Card specimen) 

By Samuel Ot. Shattock 134 

32. Achroo-amyloid liver, spleen, and kidneys 

By W. J. Hadlby, M.D. 134 

33. Acute d^eneration of liver cells supervening in the course 

of chronic cirrhosis (Card specimen) 

By F. Parkes Weber, M.D. 136 

34. Diffuse infiltration of the liver in congenital syphilis 

By H. Morlet Fletcher, M.D. 138 

35. Diffuse syphilitic change in the liver 

By F. Parkes Weber, M D. 142 

36. A case of cirrhosis of liver, apparently due to congenital 

syphilis, with thrombosis of the hepatic veins 

By T. Chxtrton, M.D. 145 

37. Thrombosis of hepatic vein associated with cirrhosis of 

the liver, probably syphilitic 

By W. S. Lazarus-Barlow, M.D. 146 

38. Liver in hepatic and portal thrombosis (Card specimen) 

By H. D. RoLLESTON, M.D. 148 

39. Cysts in the liver containing living Paramcecia coli 

By A. E. Russell, M.D., and E. F. Buzzard, M.B. 149 

40. Biliary calculi in children By George F. Still, M.D. 151 

41. Syphilitic stricture of bile-ducts (Card specimen) 

By W. S. Lazarus-Barlow. M.D. 158 

42. Tuberculous cavities in the liver [With Plate IV] 

By Herbert Morlet Fletcher, M.D., M.R.C.P. 160 

43. A case of carcinoma of the liver believed to have been 

primary in that oi^n 

By Charles D. Green, M.D , F.R.C.S. 166 

44. Atrophied pancreas from case of diabetes mellitus (Card 

specimen) By T. W. P. Lawrence 171 

45. Primary columnar-celled carcincfma of the tail of the 

pancreas (Card specimen) 

By H. D. RoLLESTON, M.D. 171 

46. Lesion of the pancreas with fat necrosis (Card specimen) 

By Cecil F. Beadles 174 

47. Sarcoma of pancreas ; glycosuria (Card specimen) 

By T. Churton, M.D. 178 

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1. Contracted kidney with multiple adenomata (Card 

specimen) By F. Parees Wbbeb, M.D. 179 

2. Small true lipoma of kidney (Card specimen) 

By P. Pabkes Webee, M.D. 181 
8. An undescended left testicle 

By Aethur Voelckee, M.D. 183 
4. Prostatic myomata and vesical calculus removed from the 
same patient (Card specimen) 

By T. Caewabdine, M.S. 183 


1. An acromegalic skull and that of a normal giant [With 

Plates V and VI] By Samuel G. Shattock 185 

2. Symmetrical senile atrophy of parietal bones (Card 

specimen) By H. Mobley Pletcheb, M.D. 195 

3. Crushed fracture of cervical spine 

By H. P. Potter, M.D. 196 

4. Central sarcoma of os calcis (Card specimen) 

By P. DB Santi 198 

5. A case of apparently aseptic suppuration of the knee-joint 

following injury, and associated with phagoc3rtosis of 
extravasated red blood-corpuscles by leucocytes 

By P. W. Andeewbs, M.D. 199 


1. Hypertrophy of the pituitary body 

By J. and T. W. P. Lawbence 202 

2. Two cases of splenic ansemia with internal haemorrhages 

in infants By G. Bebtbam Hunt, M.D. 209 

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3. Cystic disease of the supra-renal gland 

By Raymond Crawfxted, M.D. 212 

4. Cyst of the supra-renal body 

By H. D. RoLLESTON, M.D. 214 

5. Some lesions of the supra-renal in the insane 

By Cecil F. Beadlbs 214 


Epithelial tumours, probably of congenital origin [With 
Plate VII] By H. Radcliffe Ceockbb, M.D. 220 


1. Fibroma (congenital) from the neck of a child aged one 

year and eight mouths. (Card specimen) 

By H. A. Lediabd, M.D. 223 

2. Adenoma of breast associated with cyst and calcareous 

degeneration (Card specimen) 

By Cecil P. Beadles 223 

3. Cystic disease of the breast in a boy aged three years. 

By D'Abcy Poweb 225 

4. " Butter " cyst of the breast 

By H. Betham Robinson, M.S. 227 

5. A peculiar lipoma of the groin (Card specimen) 

By Cecil F. Beadles 229 

6. Large myxoma from the thigh (Card specimen) 

By H. D. RoLLESTON, M.D. 229 

7. Cysts in relation with an inguinal hernial sac in a woman 

By H. Betham Robinson, M.S. 230 

8. Multiple abdominal dermoids By A. C. Latham, M.B. 232 

9. Myeloid tumour of neck By H. J. Wabino, M.S. 232 
10. A case of multiple fibro-sarcomata of the scalp of nine- 
teen years' duration ; removal of growths ; subsequent 
recurrence in lungs 

By Philip R. W. db Santi, F.R.C.S.Eng. 234 

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11. A case of melanotic sarcoma with secondary growths of 

unusual size in the small intestine (Card specimen) 

By H. Campbell Thomson, M.D. 237 

12. Eound-celled sarcoma involving the region of the pan- 

creas, the supra-renals, liver, and left lung (Card 
specimen) By Cecil F. Beadles 239 

13. A case of umbilical papilloma which showed some activity 

of growth in a patient fifty years of age, and which 
was due apparently to the inclusion of a portion of 
Meckel's diverticulum By Charles D. G-been 243 

14. A case of substernal carcinoma 

By W. S. Lazarus-Bablow, M.D. 248 

15. Vacuolated carcinoma of the antrum 

By H. D. EoLLESTON, M.A., M.D. 249 

16. The final sequel to a case already reported of recurrent 

cystic disease of a supposed accessory thyroid 

By Arthur E. Barker 251 


1. The relations of chemical composition to germicidal action 

By James Ritchie, M.D. 256 

2. On infections by unsound meat, more especially with 

regard to the Bacillus enteritidia (Gartner) 

By Herbert E. Durham 262 

3. Congenital tuberculosis in calves 

By J. McPadyean, M.B.. B.Sc. 268 

4. Section showing a mycosis (? aspergillar) of lung of horse 

(Card specimen) [With Plate VIH] 

By Alexander G. R. Foulerton 272 

5. Blackwater, or haemoglobinuric fever 

By W. H. Crosse and W. C. C. Pakes 273 

6. Chromocyte clumping in acute pneumonia and certain 

other diseases, and the significance of the buffy coat 
in the shed blood [With Plate IX] 

By Samuel G. Shattock 279 

7. An account of some experiments upon the toxicity of 

normal urine 

By W. P. Herrinqham, M.D., P.R.C.P. 293 

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1. A case of congenital limb deficiency and redundancy 

[With Plate X] By R. Babwell 319 

2. The histology of the rheumatic nodule 

By F. J. PoYNTON, M.D., and G. F. Still, M.D. 324 

3. The technique of blood films 

By W. C. C. Pakes and R. Howaed 328 


Introductory address By Prof. Gr. Sims Woodhead 331 

S. H. C. Martin, M.D, F.R.S. . . .342 

J. W. Washboxtrn, M.D. . .344 

J. Q-ALLOWAT, M.D. ..... 345 

Professor J. McFadyean, M.B. . . 347 

A. G. R. FouLEETON, F.R.C.S. [With Plates XI and XII] 348 

W. C. C. Pakes . . . . .352 

W. S. Lazarus-Bablow, M.D. . . .353 

•F. J. Wethered, M D. . . . .357 

Professor Woods Hutchinson . . . 357 

Report of the Committee of the Pathological Society of 
London, appointed to consider the nomenclature of the 
conditions sometimes described as Pseudo-tuberculosis 361 
[J. F. Payne, M D. (Chairman), 

J. McFadyean, M.B., S. G. Shattock, J. W. 
Washbourn, M.D., G. Sims Woodhead, M.D. 
A. G. R. Foulerton (Secretary).] 

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1. On Dr. C. D. Green's ease of umbilical papilloma in a 

patient aged fifty years 

[H. D. RoLLESTON, D'Arcy Power] 247 

2. On Mr. Arthur Barker's specimen of cystic disease of a 

supposed accessory thyroid 

[J. Berry, A. A. Bowlby, S. G^. Shattock] 254 

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I. Sarcoma of pineal body with diffused melanotic sar- 
coma of the cerebrum. (Dr. C. Ogle.) (Page 4) 
II. Diphtheritic paralysis. 

Fig. 1. Cells of anterior comu at level of fifth 

cervical root in diphtheritic paralysis 
Fig. 2. Longitudinal section of left phrenic nerve of 
same case. (Dr. F. E. Batten.) (Page 

III. Epithelial pearls in the tonsil. 
Fig. 1. Three pearls in tonsil ; the middle one 

partially calcified 

Fig. 2. Epithelial pearl. (Dr. H. Walrham.) I 

(Page 65) J 

IV. Tuberculous cavities in the liver. 
Fig. 1 . A tuberculous cavity 
Fig. 2. An earlier stage in the formation of a cavity. 

(Dr. H. MoBLET Fletcher.) (Page 160) 
V. Skull of a normal giant. 
Fig. I. Front view 



(Mr. S. G. Shattock.) 

Fig. 2. Lateral view. 
(Page 185) 
VI. Acromegalic skull. 
Fig. 1. Front view 
Fig. 2. Lateral view. 
(Page 185) 
VII. Figs. 1 — 5. Epithelial tumours probably of con- 
genital origin. (Dr. Radclifpe Crocker.) 
(Page 220) ..... 

(Mr. S. G. Shattock.) 








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VIII. Figs. 1, 2. Mycosis [ ? aspergillar] of lung of ahorse. 

(Mr. A. G. R. FouLERTON.) (Page 272) 272 
IX. Chroraocyte clumping. 

Fig. 1. Action of pneumonic blood-senim on normal 

human blood 
Fig. 2. Action of the blood- serum of acute rheuma- 
tism upon the blood of a leuksemic patient 
(Mr. S. a. Shattock.) (Page 279) 
X. Congenital limb deficiency and redundancy. 

Fig. 1. Skiagram showing osseous deformities of 

left hand 
Fig. 2. Photograph showing deformities of both 

upper extremities 
Fig. 3. Skiagram showing bony deformities of right 
upper extremity. (Mr. R. Barwell.) 
(Page 319) 
XI. Results of infection with Saccharomyces tumefaciens^ 
alhus. Illustrating Mr. Foulerton's remarks in 
the discussion on Pseudo- tuberculosis. (Page 
Fig. 1. Tumour at site of inoculation fourt-een days 

after infection (natural size) 
Fig. 2. Section through tumour at site of inocula- 
tion eight days after infection ( x 600) 
Fig. 3. Section through another part of the same 
tumour ( X 600) 
XII. Results of infection with Saccharomyces tumefadens. ' 
Illustrating Mr. Foulerton's remarks in the dis- 
cussion on Pseudo-tuberculosis. (Page 351.) 
Fig. 1. Section through a secondary nodule in the 
diaphragm from same case as the last ( x 
Fig. 2. Ditto ( x 600) 

Fig. 3. Pure culture of yeast obtained from tumour 
at the site of inoculation in second rabbit 
( X 600). 



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1, 2. Sarcoma of the pineal body . . . 4 — 6 

3, 4, 5. Ulustrating central cavity in pineal body 17 

6. Neuroma of brachial plexus with molluscum 

fibrosum . . .28 

7, 8. Hypertrophied lung . . .33 

9, 10. Illustrating dilatation of the right ventricle of the 

heart . . . . 42,43 

11. Apparent thickening of the subcutaneous veins . 58 

12, 13. Congenital cyst of the base of the tongue 62, 63 

14. Adeno-lipoma of the submaxillary gland . 68 

15. Carcinomatous stomach removed during life . 107 

16. Intussusception . . . .123 

17. Crushed fracture of cervical spine . . 197 
18, 19, 20. Hypertrophied pituitary body 204, 205 

21. Effect of cold on subsidence of red blood-cor- 

puscles .... 281 

22. Total absence of right femur . . 321 

23. Rheumatic nodule . . ... 326 

Charts illustrating the toxicity of urine 316, 317, 318 

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SESSION 1898-1899. 


1. A case of embolism of both middle cerebral arteries ^ rheumatic 
endocarditis y and carcinoma of the pancreas and liver. 

By L. Fbbybebgeb, M.D. 

JK — , housewife, aged 39, was admitted to the Great Northern 
• Central Hospital on September 24th, 1898, under the care of 
Dr. Syers, complaining of wasting, occasional vomiting, and pain in 
the abdomen. She had suffered a great deal from rheumatic pains, 
but was never laid up with rheumatic fever. She had had several 
children at term and two miscarriages. 

On admission the patient was very pale and thin. There was a 
faint blowing murmur during the diastole over the base of the left 
ventricle and at the apex ; the area of heart dulness was not in- 
creased ; the apex-beat was somewhat heaving ; pulse 87, regular ; 
respirations 18, regular ; there were no other abnormal physical 
signs in the chest. In the abdomen, across the middle line, about 
three inches above the navel, a transverse oblong tumour could be 
felt, which was not moveable or tender on pressure. The liver was 
considerably enlarged, its surface smooth ; the spleen reached the 
anterior axillary line, and was hard and tender on pressure. The 
urine contained no abnormal constituents. There was considerable 
constipation, and the patient complained of feeling sick. 

Two days after admission, while in bed, the patient was suddenly 
taken ill with vomiting and griping pain in her abdomen. A few 


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moments later it was noticed that she was aphasic and paralysed 
on her right side; the paralysis and aphasia were complete, but 
the patient was not unconscious. There was also a slight rise of 
temperature up to 100® F., which subsided after a couple of days. 
The patient gradually regained her power of speaking, but the 
extremities of the right side remained completely paralysed. 

On October 9th the patient suddenly became quite stuporous, 
and remained so until her death, lying motionless on her back. 
Death occurred nine hours after the onset of the stupor. 

At the poat-mortem examination, ten hours after death, the 
following conditions were found : 

Eigor mortis present ; body much emaciated, ashy pale ; exten- 
sive, pale, livid poat-mortem stains on tlie back of the trunk and 

The left parietal bone externally bears a roundish, button-like 
bony excrescence; the bones of the skull are twice as thick as 
normal and as hard as ivory; the dura mater very adherent to the 
vitreous table ; the grooves for the meningeal arteries very deep 
and tortuous. 

The pia-arachnoid over the whole convexity and at the base 
thickened and slightly turbid, especially over the two central 
sulci. The left middle cerebral artery, at the spur formed by its 
division into three branches, is blocked by a small reddish-grey 
embolus, the size of a millet seed. In front of the embolus is a red 
thrombus, which is continued in a centripetal direction into the 
insertion of the frontal branch of the middle cerebral artery. The 
clot is firmly adherent to the vessel wall, dry and friable. The 
right middle cerebral artery contains a reddish-grey embolus, the 
size of a rice corn, situated at the ramification of the middle 
cerebral artery into the four branches, which are continued on to 
the frontal and occipital lobes and the island of Reil and the 
operculum. The embolus is continued centripetally by a dark 
red thrombus about half an inch long, with a paler whitish-grey 
tapering proximal end, which reaches as far as the anterior com- 
municans artery. This clot is firm, not adherent to the wall of the 
artery, and consequently preserves its cylindrical shape. Beyond 
the emboli the arteries were completely empty. 

The substance of the left parietal lobe was considerably softened 
and the convolutions flattened ; the changes on the right side were 
less obvious. The brain was not dissected. 

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The lung$ were natural. 

The heart was small, with a considerable amount of subepicar- 
dial fat. The mitral valves showed old fibrous thickening and two 
patches of recent endocarditic vegetations. The aortic, pulmonary, 
and tricuspid valves were natural. There was no atheroma of the 
aorta or large vessels. 

The liver was large ; it contained many metastatic deposits of 
carcinoma, of various sizes, both in its substance and under the 
peritoneum. The consistence was increased, the surface smooth. 

The gdllrhladder was natxiral. 

The spleen is enlarged to twice its normal size, and contains two 
small ansemic and one large hsemorrhagic infarct. 

The pancreas, in its middle third, contains a large primary 
carcinoma, which is very hard and fibrous. The glandular struc- 
ture of the tail and head of the pancreas is perfectly normal, but 
the duct contains several cystic dilatations. The growth of the 
pancreas was adherent externally to the stomach without encroach- 
ing upon its muscular coat or mucosa. 

The stomach was perfectly natural. 

The kidneys were large and firm, their capsule somewhat 

The intestinal canal, bladder, and genital organs were natural. 

No signs of syphilis could be found. 

Points of interest:— 1. The occurrence of an embolus in each 
arteria fossse Sylvii. 

2. The combination of carcinoma and endocarditis, which is by 
no means of frequent occurrence. 

3. The different appearance of emboli 1 and 2. 

Embolus No. 1 is fourteen days old. The thrombus attached to 
it is dry, brittle, and firmly adherent to the endothelium of the 
artery. It is also somewhat reduced in size, owing to the absorp- 
tion of its liquid constituents. Its colour is dark brick-red. 

Embolus No. 2, nine hours old, is succulent, of dark purple 
colour, not adherent to the inner coat of the artery. It conse- 
quently retains its shape when the artery is cut open, whereas 
No. 1 is broken up into a number of parts which adhere firmly to 
the wall of the artery. (Cf . paper " A Brain with Three Consecutive 
Hssmorrhages," 'Path. Soc. Trans.,' vol. xlix.) 

November \6th, 1898. 

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2. (1 ) Sarcoma of pineal body, with diffused melanotic sarcoma of 
the surface of cerebrum. (2) Tumour of pineal body in a boy. 

Bj Cykil Ogle, M.B. 
[With Plate I.] 

CASE 1. — The first specimen shown is a woman's brain of a very 
unusual appearance, looking as if the 8ui*face had been 
painted over with sepia and black-lead, or Indian ink. The whole of 
the cerebrum is covered in this way, but the cerebellum and pons 
were not; the discoloration is far more marked over the upper 
and latenil surfaces than at the base. 

Beneath the microscope it is seen that the meshes of the pia 
mater are occupied by melanotic sarcoma, the cells of which are 
chiefly of a spindle shape, and granules of brownish-black pigment 
are abundant within them. This growth is spread in a fairly 
uniform layer over the convolutions, dipping down into the sulci 
and invading the grey matter, apparently along the sheaths of the 
fine vessels entering the cortex, so that within the cerebral sub- 
stance are fine tracts and little islands of melanotic growth, the 
cells of which, in transverse section, usually have a laminated or 
concen trie arrangement. 

Deep in the substance of the hemispheres are to be seen also a 
few nodules of growth, of the size of small peas. 

Fig. 1. 

A s sarcoma of the pineal body split in two, and two halves turned aside. 

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Illustrating Dr. Cyril Ogle's case of Sarcoma of tbe Pineal Body, 
with Diffused Melanotic Sarcoma of the Cerebrum, in a woman. 
(Page 4.) 

Showiog the melanotic sarcoma spreading over the cortex and invading it. 

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In the position of the pineal body is a globular tumour, 
measuriDg about 1^ inches ia diameter, pressing aside the optic 
thalami, which, as well as the corpora quadrigemina, are distorted 
and slightly invaded by the growth, as shown by their black 
colour. The tumour is in the middle line, and was attached in the 
region of the pineal body, but not elsewhere. 

Microscopically this growth is also a sarcoma composed of cells 
of all shapes, some giant-cells, but chiefly of spindle-cells of 
medium size : granules of pigment are visible in some of the cells, 
but there is much less pigmentation than in the difEuse growth 
over the cortex. 

There were no other growths in the body, which was in all 
respects otherwise healthy. 

It would thus seem that the diffuse condition of melanotic 
sarcoma invaded the surface of the brain along the pia mater from 
the primary growth of the pineal body. 

Ziegler describes an alveolar sarcoma or endothelioma of the 
pia mater, occurring sometimes as a diffused growth over the 
brain, which, he says, is rarely pigmented, and the cells of which 
are highly developed, and resemble polymorphous epithelioid cells 
of carcinoma; but the present example would appear not to be 
primary in the membranes, although thus diffused, and the cells 
are those of a mixed-celled sarcoma with pigment in remarkably 
large amount. Dr. Byron Bramwell, in his book on ' Intra-cranial 
Tumours,' gives several plates of a brain of exactly similar aspect, 
from a diffused layer of melanotic sarcoma ; but in his case it does 
not appear n^ hether there was any primary growth in the pineal 
region, and the details of the case are not given ; nor are they, I 
believe, to be found elsewhere at present. 

The patient was a woman aged 32 years, and was under observa- 
tion for about ten weeks. Her illness began definitely with a 
sudden state of unconsciousness, accompanied by right-sided para- 
lysis. For a few weeks previously, however, she had been excitable 
and irritable, with occasional pain in the head ; she had complained 
also, sometimes, of shaking and numbness of the right hand. 

Her symptoms after the first fit, apart from headache, emaciation, 
choked disc, and dulness of intellect ending in coma, were inter- 
mittent aphasia and right hemiplegia, which would last a few days, 
then clear up, to return again in a few days ; eventually the right- 
sided hemiplegia became permanent. 

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Throughout her illness there appears to have been only one con- 
vulsive attack, which is described as affecting all the parts of the 
body. That there were not more convulsions seems remarkable 
when one considers the wide extent of the infiltration of the cortex 
by the new growth. 

Case 2.~In the other example shown this evening, a globular 
lump of about 1 inch in diameter is seen occupying the position of 
the pineal body, and projecting forwards into the third ventricle; 
the optic thalami are somewhat pushed aside, and their posterior 
parts hollowed out, but not invaded. The tumour is adherent to 
the velum interpositum, which is stretched over it, and the corpora 
quadrlgemina are obviously flattened, and the nates a little 
hollowed out by the growth above them ; but the latter does not 
seem to have infiltrated any of the parts around, and is attached 
only in the position of the pineal body. 

There were no other growths in the body, all the organs of whicb 
were healthy. Excepting for some excess of fluid in the ventricles 
and at the base, the brain was otherwise healthy. 

The pituitary body was natural in appearance. 

Fig. 2. 

.^v,>.*-— c 

Illustrating Dr. Cyril Ogle's case of pineal tumour in a boy. (Drawn by G. H. 
Goldsmith, M.B.) a. The tumour of pineal body, covered by velum inter- 
positum, and projecting into the third ventricle (a) ; it has pushed aside the 
corpus striatum (b). and the optic thalamus (f), and pressed upon the 
corpora quadrigemina (d). c. The cerebellum, divided and turned aside. 
B. Superior medullary velum covering the fourth ventricle (h). 

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On section the tumour is seen to be largely composed of blood, 
which is coagulated and mixed up with tracts of soft grey material, 
like new growth. 

Beneath the microscope the constitution of the growth is a little 
difficult to make out; apart from blood there are strands of 
connective lissue, and collections of small cells with interlacing 
processes — an appearance very similar to that found in the normal 
pineal body. There are, however, in addition, alveoli full of ex- 
ceedingly large and vacuolated nuclei, the bodies of the cells of 
which appear to have coalesced; under a low power these have 
somewhat of the appearance of giant-cells lying close together, but 
under a higher power might suggest small islets of cartilage ; per- 
haps on the whole they are more likely to be large and rapidly 
proliferating cells ; they are most evident close to blood canals ; the 
latter are large and very numerous. There are also rounded spaces 
of considerable size, bounded more or less regularly by connective 
tissue, and containing an inner lining of cells of a columnar shape 
with bold nuclei ; the cells being arranged endways like a palisade, 
the rest of the space being, in part at any rate, occupied by an in- 
definite material staining a faint purple by Yan Gieson's method. 
Perhaps the tumour may best be described as an alveolar sarcoma 
with haemorrhage and cysts. 

But the spaces mentioned above, which are lined by columnar 
epithelium, are, I think, difficult to interpret ; it is just possible 
that these cells may represent a rudimentary retina, to the cells of 
which, as depicted in some forms of pineal eye by Baldwin Spencer, 
they are somewhat alike ; or, more probably, these spaces lined by 
epithelium may represent the state of the body found in birds — 
that of saccules, with albuminous contents, lined by epithelium. 

The symptoms in this case were exceedingly interesting. The boy 
(P. W — ) was six years old, and was in hospital for five weeks, until 
his death. He had been well until a few months before admission, 
but during these months his father noticed that he was strange in 
manner, was given to masturbation, and inclined to sleep a great deal. 

On admission he was well nourished ; his gait was staggering, 
but there was no paralysis anywhere ; the reflexes were normal ; 
there was no tremor ; the back, especially the back of the neck, was 
held stiffly. His eyesight was good. The boy's penis was of large 
size, fully equal to that of a lad of sixteen or seventeen years ; pubic 
hair was fairly plentiful, but the testicles did not seem enlarged. 

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Until his death, a few weeks later, he had frequent attacks of 
vomiting, and frequent fits, marked especially by opisthotonos; 
but the most striking symptom was sleepiness. He would sleep 
night and day, almost continuously, but could be easily roused by 
a question and slight shaking, and then would answer with perfect 
readiness and intelligence, but would fall asleep again if left alone. 

About ten days afterwards the pupils were only slightly active 
to light, and were large, but variable in size ; the boy saw perfectly. 
There was some loss of power in external rectus of the left eye. 

About a week subsequently both external recti were inactive, the 
pupils widely dilated and inactive to light, and the boy quite blind. 
Although no choking of the disc was to be seen, there was slight 
pallor and blurring, as from optic neuritis of slight degree. 

There was throughout his illness no ptosis, nor evidence that 
any other muscle of the eyes except the external recti was 
paralysed. There was never any paralysis of face or muscles of 
the limbs or body. There was no deafness nor loss of sense of 
touch. There were no pelvic symptoms, excepting some priapism. 

Until death he remained in a state of continuous sleep, from 
which he could be easily roused. He never complained of headache 
when asked, but of pain in neck and back if disturbed from his 
rigid position. He remained quite blind, and neither eye would 
move outwards beyond mid-line. Vomiting was frequent, so also 
were fits, in one of which he died. No other fresh symptom arose. 
The knee-jerks, at first present, were soon absent, and remained so. 
There was no rise of temperature and no wasting. 

Remarks, — Tumours of the pineal body appear to be very rare ; 
hyperplasia, psammoma, and cystic degeneration, according to 
Ziegler, being the least uncommon. 

Wilks and Moxon, in their * Pathological Anatomy,' state that 
cystic disease, in their experience, is not uncommon, and appa- 
rently often unaccompanied by any symptoms. 

Of tumour, two cases have been recorded in the * Transactions * of 
this Society : the first fcy Dr. Turner, in vol. xxxvi ; the second by Dr. 
Coats, in vol. xxxviii. The latter, besides referring to Dr. Turner's 
case, mentions three others, by Weigert,^ Falkson,* and Ziegler.* 

In all of these the constitution of the tumour was complex. 
Thus in Weigert's specimen, which he describes as a teratoma, 
1 'Virchow's Arch.,' vol. Ixv, p. 212. « Ibid., vol. Ixxv, p. 550. 

• Ziegler, • Lehrbuch der path. Anat.,' 4th edit., vol. ii, p. 618. 

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were muscle, hair, fat, cysts, aud cylindrical epithelium. In Falk- 
son's, besides spindle-celled sarcoma, were cartilage and cysts 
lined by cylindrical epithelium ; and Dr. Coats's example was very 
similar, excepting that the arrangement of cylindrical epithelium 
was such as to suggest glandular structures. In Ziegler's,- appa- 
rently sarcoma, and again cysts lined by cylindrical epithelium. 
In Dr. Turner's, collections of large cells termed carcinomatous, 
together with sarcoma, and other cells which were regarded as 
polar nerve-cells. 

In addition to these five I have found reference to three other 
cases. Dr. Duffin ^ reports a case of apparently a solitary glioma, 
and with symptoms somewhat similar to those of the boy narrated 
to-day, namely, a staggering gait, stifEness of muscles at back of 
the neck, drowsiness for a month, with intellect unimpaired ; in 
addition, however, with some paralysis of third, seventh, and 
eighth nerves, perhaps due to pressure downwards upon the floor 
of the aqueduct. 

Dr. Blanquinque,2 of Laon, describes an hypertrophy of the 
pineal body to the size of a pigeon's egg, with hfismorrhagic extrava- 
sations and calcareous points. Fits, paraplegia, and amaurosis 
were present ; but the clinical history is scanty. 

Gutzeit ' relates the case of a boy with a tumour of the pineal 
body, in part cystic, but containing also fat and muscle, both 
striped and unstriped. No clinical details are given. 

Thus of these eight cases two may be perhaps described as 
hypertrophy or glioma ; the remaining six are all more or less 
complex in composition, but most of them contain sarcoma tissue. 
One may remark in this connection also, in one of the specimens 
now being shown, the large amount of pigment in the sarcoma cells ; 
for, although I have been unable to find pigment in the normal 
pineal body in man, it is very abundant in the pineal eyes of 
lizards — in the retinal elements, the lens, and in parts aroimd the 
optic vesicle ; as, of course, it is in the choroid and retina of man. 

The pineal body, it is well known, appears in development as a 
hollow outgrowth of the posterior portion of the fore-brain, or 
thalamencephalon ; and in some of the lower forms of animals 
this hollow outgrowth becomes elaborated into a structure evidently 

* * Clinical Society's Transactions,' vol. ix. 

3 « Gazette hebdomadaire,' 1871 ; ' Lancet/ 1871. 

' * Inaugunil Dissertation,' K&nigsberg, 1896. 

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a median eye, with a very perfect lens, retina, optic nerve, and 
pigment, as shown more especially by Baldwin Spencer in the case 
of lizards. Although no doubt functional as an eye in extinct 
forms, it is probably not so in any living animal ; and in mammalia 
it exists in a very degenerate condition. 

As far as one can learn from descriptions and from sections, the 
pineal body in man is solid, divided into loculi by fibrous parti- 
tions, holding blood-vessels; the divisions are filled with a fine 
reticulum holding nucleated cells of a uniform and small size, the 
branches of which cells appear to form the reticulum. There does 
not seem to be any pigment in the body. 

It is not obvious that it contains any nerve-fibrils, but other 
modes of staining might demonstrate them if present. Nerve- 
fibres are, however, described in the stalk of the pineal body. 

The entire structure of this body is, in appearance, exceedingly 
like compartments of neuroglia ; but it is also very like some 
layers found in the grey matter of the cerebellum, the cells of 
which are, I believe, regarded as nerve-cells. 

As far as I am aware no special nervous functions are attributed 
to the pineal body, although I see that extracts of it are sold, to 
be administered '' in functional diseases of the brain due to failure 
of nutrition ; in cerebral softening ; chronic mania, and dementia." 

Ferrier, however, in his book on the ' Functions of the Brain ' 
passes it over in silence. 

Neither, if one looks to its development as representing a 
median eye, would one expect that any nutritional changes in the 
|K>dy at large would be produced by disease in the pineal gland, 
such as apparently follow disease of the anterior lobe of the 
pituitary body, or of the thyroid gland ; since the pineal body does 
not represent structures with a glandular, secretory, or excretory 
function, as is probably the case with the thyroid and pituitary 
bodies. Even in its most perfect form, as presented in lizards, no 
epithelial structures, properly so called, would seem to be present; 
although, of course, as an outgrowth from the brain it is ulti- 
mately epiblastic in origin. 

The cases now related do not, I am afraid, throw much light 
upon the question (if it be a question) whether the pineal body 
possesses in man any special function. 

As regards the woman, there was such wide-spread growth that 
any symptoms referable to the tumour of the pineal body would 

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be obscured bj the general or diffuse symptoms present ; and the 
earlier part of the history is very defective. 

As regards the boy, whore growth was limited to the pineal 
region the symptoms were, no doubt, for the most part due to 
pressure on adjacent structures, and more especially on the 
corpora quadrigemina. 

Ferrier's experiment of destroying just the surface of the 
superior tubercles of the corpora quadrigemina in monkeys 
resulted in total blindness, dilated and inactive pupils, without 
ptosis ; there was perfect sensation, no paralysis of the body, but 
an entire inability to maintain a normal equilibrium, or to move 
steadily. All these were prominent symptoms in the boy. His 
blindness was of exceedingly rapid onset, and accompanied by very 
slight change in the fundus of the eye, thus suggesting inter- 
ference with sight tracts or centres ; moreover, there was no pupil 
reaction to light. 

There was apparently no paralysis of the third nerve, as far as 
could be ascertained, and certainly no ptosis, but the movement 
outwards of either eyeball was not possible. 

Perhaps one may account for this as a loss of the " conjugate 
movement " of the two eyes, the path for which, from the cortex 
to the nucleus of the sixth nerve, according to Gowers, traverses 
the corpora quadrigemina. It could, I think, hardly be due to 
direct pressure on the sixth nerve, or its nucleus, on each side, 
seeing that the third and the seventh were normally active, and 
that there was no interference with the pyramidal tracts. 

Two, however, of the symptoms in the boy's case appear, to 
some degree, unaccounted for — the continuous sleep, and the 
precocious development and enlargement of the penis. The latter 
presented a very striking and even embarrassing appearance in 
one so young. And the enlargement of what may be described as 
an extremity, in conjunction with the general symptoms of an 
intra-cranial tumour, with also the blindness and interference with 
eye muscles, led me to suggest, during life, a diagnosis of tumour 
of the pituitary body. 

The sleepiness could in no sense be called coma ; the boy could 
be easily roused from it, and was then perfectly intelligent. 

As regards the former of these two symptoms, I have not seen 
any notice in the records of those cases of pineal tumour where 
details of clinical history have been given, of any special nutritional 

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changes in the general body ; ^ but, as regards the other symptom, 
I find that in Dr. Coats's case sleepiness was present, and 
lasted for several months ; and drowsiness for a month is men- 
tioned in Dr. Duffin's case. Perhaps this symptom might prove 
to be of value in the localisation of pineal tumour, although it 
may not be directly due to disease of the pineal body, but rather 
to the position of the growth and interference with surrounding 
structures. December 6th, 1898. 

3. Tumour of the pineal body. 
By T. W. P. Lawrence. 

THE specimen consists of the medulla oblongata, pons, and part 
of the mid-brain, with the pineal body, from a boy who died 
of tuberculous meningitis. The pineal body is enlarged to several 
times its normal size, and is somewhat altered in shape. Its 
outline, viewed from above, is almost circular, and its diameters 
measure 14 mm. ; the organ is compressed from above down- 
wards, and measures in this direction 7 mm. The central part 
of the upper aspect is slightly depressed over an area measuring 
6 mm. across, presenting an umbilicated appearance. The 
under aspect is nearly flat. The circular margin is broad and 
rounded. Both surfaces and margin are smooth, and present 
evidences of slight lobulation. The organ is free from adhesion 
to surrounding parts, and presents nothing abnormal as regards 
its colour. On cutting into it, it was found to be soft, solid, and 
free from brain-sand. A portion was removed for microscopic 
purposes from the upper part of the organ, along the median 
plane, but not quite including the whole thickness of the organ. 

Under the microscope two main zones are distinguishable, a 
narrow one lying at the periphery of the organ, and a central one 
including the larger portion of the section. The peripheral zone 
is broadest at the anterior part of the organ, and is composed of 

^ Bearing on this question, the following case has subsequently been recorded 
by Heubner (' AUg. med. Central. Zeitung,' An. 28, S. 89). In a boy aged four 
and a half, the penis, scrotum, and testes were abnormally large, and the pubic 
hair fully grown. Growth had proceeded normally until he was seven and a 
half months old. The excessive growth took place in one year. There were, at 
the same time, slightly choked discs, and symptoms of paralysis. Post mortem 
a tumour of the pineal gland was found. 

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cells of considerable size closely aggregated together in parts, and 
haying large oval and deeply staiuing nuclei, but the outlines of 
the cells are indistinct owing to degeneration of their protoplasm. 
The cells of this layer are evidently pineal eeUa, The central zone 
of the section is composed of finely granular material, staining 
slightly. The masses of granules, evidently products of degenera- 
tion, are disposed in a somewhat reticulate fashion, and an open 
network of delicate connective-tissue fibres is seen tmversing them 
in many parts of the section. No cells or cell nuclei are present 
in this zone, which doubtless consists of the remains of a tissue 
which by its degeneration and shrinking has produced the umbilica- 
tion of the upper surface of the pineal body. Between these two 
zones there is towards the anterior end of the organ a third zone, 
consisting of a well-staining tissue, composed of a close network of 
very delicate interlacing fibrils and scattered cells of small size, 
round or triangular in shape, with scanty protoplasm and round 
and deeply staining nuclei. This layer appears to be closely con- 
nected with the central degenerated portion on the one band, and 
on the other hand it is not sharply marked ofE from the pineal 
tissue of the periphery, but is prolonged into the latter, and divides 
it up into distinct areas. From the histological characters of this 
third zone it is concluded that the enlargement of the organ is 
due to a gliomatous growth, and that the central part of the 
tumour has undergone degeneration. 

The patient, a boy aged 16, was under the care of Dr. Bradford 
in University College Hospital. His illness commenced with a 
cough, which, however, improved, but was succeeded by pains in 
the head, which commenced ten days before death. Pain in the 
chest and abdomen set in soon after, and vomiting was present 
during the last four days of the illness. Delirium commenced 
three days before death. On admission to the hospital on the day 
previous to his death the patient was semi-conscious, with face 
flushed ; very irritable and crying out on being moved. Breathing 
was heavy ; respirations 28 in the minute. The pulse was slow 
and full. The pupils were widely dilated, and did not react to 
light. Strabismus was present at intervals. There was total 
blurring of the right optic disc, with large and tortuous veins ; 
the left disc was affected on the inner side only. The limbs were 
in constant movement of an athetotic character, but there were no 
convulsions. The abdomen was moderately distended. A few 

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hours before death the patient became completely comatose, and 
the breathing stertorous. Resp. 48 ; pulse 136 and regular. Great 
rigidity of the back muscles was present. The temperature ranged 
from 102-2*^ to 105°. There was nothing noteworthy in the family 
history and general history of the patient. Up to the time of the 
present trouble he had had good health, and was free from illnesses. 

Post'Tnortem examination. — The veins on the surface of the brain 
were distended, and the cerebral ventricles were very full of clear 
fluid. A small patch of purulent matter was present over the 
margin of one parietal lobe, and there was pus in small amount on 
the upper surface of the cerebellum. The velum interpositum and 
the adjacent part of the membranes covering the cerebellum were 
much thickened by a deposit of inflammatory exudation, but the 
pineal body was not involved. Purulent matter was present over 
the base of the brain from the optic nerves backwards, and 
extended into the Sylvian fissures, where discrete tubercles could 
be distinguished. 

The left lung was universally adherent; two or three small 
infarcts were present in the right lung. No tubercles were present 
in either lung. Some of the bronchial glands were caseous. The 
mesenteric glands were healthy. The heart was healthy. The 
right kidney was completely atrophied; the left healthy, and 
weighing 7i oz. The liver was universally adherent. The spleen 
was healthy except for the presence of two or three tubercles on 
its surface. December 6th, 1898. 

4. Pineal cyst. 
By A. E. Garbod, M.D. 

THE specimen shown is a portion of the brain of a boy aged 16, 
who died of diabetes. 
At the post-mortem examination, which was made thirty-five 
hours after death, a small cyst, as large as a pea, was found in the 
pineal body. The walls of the cavity were smooth, and had a 
yellowish tint. No hfismatoidin crystals were found in the cavity. 
The fourth ventricle and the rest of the brain appeared natural. 

The pancreas was unduly small, and was found, on micro- 
scopical examination, to be markedly fibrotic. 

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The liver and kidneys were fatty. 

It seemed possible that the pineal cyst was of a similar nature 
to those which are described as occurring in other parts of the 
brain in cases of diabetes; but its close resemblance to pineal 
cysts found in other than diabetic patients throws doubt upon this 
view. December 6th, 1898. 

5. Cysts of the pineal body. 

By A. E. EussELL, M.D. 

IThe patient in whom this cyst was discovered was admitted 
• in a comatose condition, from a fractured base of skull, into 
St. Thomas's Hospital in September, 1898, under Mr. Anderson's 
care. He was twenty- three years old. Post mortem the pineal 
body was found to be distended into a thin-walled cyst five eighths 
of an inch in diameter. The cyst contained clear albuminous fluid. 
At its attached portion the wall was opaque, but at the free 
extremity the wall was so thin as tx) be translucent. No other 
lesion was present. Careful inquiry among his relatives failed 
to elicit any symptoms referable to the condition. 

2. Specimen from the museum, St. Thomas's Hospital.^ In this 
specimen the pineal body was converted into a cyst of about a 
third of an inch in diameter, the wall of which contained much 
earthy substance. The cavity was filled with clear and amorphous 
granular material. No clinical record. December 6tht 1898. 

6. Notes of two cases of dilatation of the central cavity or 
ventricle of the pineal gland} 

By A. W. Campbell, M.D. 

CASE 1. — The patient was a female epileptic aged 33, who died 
of phthisis. There was no noteworthy lesion in the brain» 
and it was one of average development, but the pineal gland was 
> No. 2080. 
* Both these cases occurred in Rainhill Asylum. 

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strikingly enlarged, measuring 10 mm. in the transverse direction, 
13 mm. in the sagittal direction, and 8 mm. in depth ; its general 
shape was round, but it was pointed posteriorly. 

The whole body was hardened in formalin 5 per cent, and then 
in alcohol, and after embedding in celloidin serial sections were 
made in the vertico-sagittal direction. Every section was mounted 
and stained by the method of Yan Gieson or with toluidin blue. 

The sections showed that the enlargement of the gland was due 
to a remarkable cyst-like dilatation of its central cavity or ventricle. 
The cavity was situated more or less centrally ; it contained glairy 
brownish fluid, had a brown lining, was of ovoid form, and its 
diameter was 8 mm. in the horizontal direction and 6 mm. in the 
vertical direction. The wall of this cavity varied in thickness 
between 1*5 and 2*5 mm., being thickest posteriorly ; to the naked 
eye it seemed to possess the brown-pink colour of the normal 
gland, but microscopically it could be resolved into two layers. 
The outer of these layers was on the whole thinner than the inner, 
and was composed of the cellular substance of the normal pineal 
body, the groups of cells being separated into islets by septa of 
pia mater. It stained deeply with hsematoxylin, and in it corpora 
arenacea — sometimes simple, sometimes compound — were scattered. 

The composition of the inner layer was very different from that 
of the outer, but as it stained indistinctly it was difficult to deter- 
mine its precise nature. However, close examination under a well- 
illumined oil-immersion lens revealed the presence of numbers of 
large, very pale, or faintly granular cells of round or oval form, few 
of which contained a nucleus, and then only a comparatively small 
faintly stained one. Similar cells, but of flattened form, could be 
seen in places along the inner lining of the cavity. What the exact 
nature of these cells is I am not prepared to say. 

Then scattered all over the field in this inner layer were large 
cells or bodies of varying shape, some irregular, some round, some 
oval, which were filled with coarsely granular dark brown pigment, 
and in some of these one or more nuclei could be clearly seen. 

Lastly, the most remarkable feature of the sections was the 
existence of a dense collection of these pigmented bodies, situated 
on the inner lining of the cavity and projecting slightly into it at 
its posterior extremity, the pigmented bodies being arranged in 

In regard to the nature of these bodies, it is possible that they 

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Pig. 8. 

Fia. 5. 


Fig. 4. 

JVbrmal gla/id 
substance. ^^- 

ZfV^ fji^ 0/ cavity. 


Fig. 3. — Dilatation of central cavity of pineal gland. Natural size. The 
apper two drawings show the cavity laid open. The lower two show the outer 
surface of the pineal body. 

Fig. 4. — Collection of pigment on inner wall of cavity of pineal gland. 

Fig. 5. — 1. Collection of cells seen on the inner surface of wall of the cavity 
2. Cells seen in the substance of the inner layer of the wall. 3. Pigment-ed 
bodies or cells seen in inner layer of wall. 


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are merely collections of hsematoidin crystals which have become 
darkened by age, or, on the contrary, they may be pigmented cells 
analogous to those usually present in the choroid and retina of the 
eye, I believe that the latter assumption is the correct one, and if 
it be so, it is a proof that the pineal gland is really a rudimentary 
organ of sight, and it will also explain the origin of a primary 
melanotic sarcoma in that body. 

Case 2. — The second specimen was also taken from the brain of 
an epileptic female. To the naked eye it was similar in all respects 
to the above, but the enlargement of the cavity was somewhat 
greater. Unfortunately it was not submitted to microscopic exami- 

I have recently obtained a third similar specimen, but have not 
had time to examine it. 

I would add that these notes have been hurriedly put together 
for this meeting, and that my observations on this pineal change 
are far from complete. December 6th, 1898. 

7. The pineal gland ; its normal structure ; some general re- 
marks on its pathology ; a case of syphilitic enlargement. 

By John E. Lord, M.B., introduced by Mr. Beadles. 

fPHB pineal gland is a portion of the brain of exceptional interest, 
-^ and it is the intention of this paper to describe the normal 
naked-eye and microscopical features and one pathological de- 
parture. Without entering into details, the following points 
appear to me to sum up the present position of our knowledge in 
general, as regards the pineal gland in health and disease. 

1. The pineal gland or epiphysis cerebri is a rudimentary struc- 
ture, and is developmentally the representative of the median eye 
present in some animals (Anguis, Hatteria, <&c.). 

2. It is functionless in man. 

3. Being in man a useless, decaying structure, its normal condi- 
tion is always more or less a pathological one. 

4. It has, per «6, pathological potentialities, mainly of two kinds: 

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(a) New growth, from the presence of cells of an embryonic 

(h) The degenerative processes constantly present may become 
unduly active and exaggerated, and may result in cystic dis- 
ease, &c, 

5. It may be affected pari passu by morbid conditions afEecting 
the brain generally. 

6. When actively diseased its symptoms are those which result 
&om pressure on the surrounding parts. 

Normal structure : ▲. The pineal gland is divided into a number 
of loculi by an irregular network of septa. These septa are com- 
posed of small fibres (like white fibrous tissue), in the midst of 
which are scattered spindle and oval cells. This tissue is in part 
derived from the two pineal peduncles and partly from the pial 
investment, the latter supplying small blood-vessels and lymphatics. 
The loculi have no endothelial lining. They contain a stroma of 
fine fibres which appear to be the processes of small branching 
cells similar to those found in adenoid tissue. In this meshwork 
are crowded cells of various shapes, some of which are pale, others 
being filled with granules. There is also a ground substance of 
some gelatinous material which stains faintly, and in which can be 
seen the debris of cells which have broken down. 

B. The following changes occur normally : 

1. Calcification of septa, — This usually occurs centrally and 
towards the apex, and gives origin to the so-called " brain sand.*' 
Lime crystals can be seen in the septa in other parts of the 

2. Formation of amyloid bodies. — In some of the loculi, usually 
near the apex, the granular cells undergo a process of amyloid 
degeneration, the granules swelling up and forming a pale yellow 
material. The cells so affected unite together and form a nodular 
body of a pale yellow colour which fills the loculus. These amyloid 
bodies take on the aniline stains readily. 

c. "A normal cavity." A normal cavity in the pineal gland 
has been described. Its existence, however, is much to be doubted. 
The only cavity I have found is that produced by the calcification 
of the septa, and the subsequent union of the loculi. There may 
be one large cavity or several small ones. Such, however, cannot 
be considered normal in the ordinary sense of the word ; it is a 
condition produced by a process of degeneration. 

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Variation in shape and size. 

The normal pineal gland is commonly conical in shape. When it 
enlarges it expands in the direction of the least resistance, which is 
posteriorly and laterally. Wlien only moderately enlarged it 
becomes heart-shaped, but when greatly enlarged it is the shape of 
a broad spade. 

The actual size varies very much, and does not depend upon the 
size of the whole brain. The following dimensions are based upon 
the measurement of a number of glands which could be considered 

Length 5 — 9 mm. 

Breadth 3—8 „ 

Thickness 2 — 4 „ 

A case of syphilitic enlargement. 

In this case the dimensions of the gland were — 

Length 21 mm. 

Breadth 16 „ 

Thickness 9 „ 

Its pial investment was congested and oedematous, and in its 
substance were two large calcareous nodules. Microscopically 
considerable alteration had occurred in its structure. There was a 
vast increase in the number of cellular elements in the septa, and 
also a formation of new septa, the latter dividing the gland up 
into extremely small loculi. In some places the loculi seemed 
actually obliterated. These cells stained deeply, and each had a 
large nucleus. The condition appeared to be a hypertrophic 

Clinically the case presented no symptoms which could definitely 
be put down to the morbid condition of the pineal gland. She was 
a woman who had been insane for some seven years, having during 
that time recurring epileptiform convulsions and tits of violence. 
She eventually became paralysed on the left side, the paralysis 
afterwards affecting the right leg. For some time before her death 
she was very demented and in a state of partial stupor. The 
stupor, however, cannot definitely be put down to the pineal con- 
dition, because it is so common a symptom of advanced cerebral 
disease. Post mortem a growth was found in the right central 

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region of cerebrum, a second one being situated at the tip of the 
occipital lobe on the left side. 

A microscopical examination of the growths confirmed the pre- 
vious diagnosis of gummata. There was degeneration of the 
pyramidal tracts in the cord. December 6th, 1898. 

8. Sarcomata involving the spinal cord of a child aged three 
years, {Card specimen.) 

By F. E. Batten, M.D. 

THE child first came under observation in November, 1897, with a 
sore on the lower part of the back, and a history of weakness 
in the legs of three months' duration. Six months later the child 
was completely paralysed in the lower limbs, whicli were rigid in 
the flexed position ; the knee-jerks were present, no ankle-clonus 
<^uld be elicited, and the plantar reflexes were absent ; there was 
loss of sensation to the level of the fifth rib, and the intercostals 
were paralysed below this level. There was a small growth lying 
to the left of the spine at the level of the fifth dorsal vertebra. The 
child died three months later, the knee-jerks not being obtained 
during the last fourteen days of life. 

At the autopsy a large mass of growth was found to the left of 
the bodies of the vertebrae in the dorsal region ; it had extended 
into the spinal canal and involved the dura mater and the cord to 
the most marked degree at the level of the fifth and sixth dorsal 
vertebrae ; the growth, however, extended up to the third cervical 
segment, and below to the level of the eighth dorsal. There were 
masses of growth in the dura mater, and these had caused erosion 
of the skull ; another growth was found in the right femur, the 
primary growth being that in the thorax. 

On microscopical examination the growth proved to be a small 
round-celled sarcoma. There was almost complete destruction of 
the cord in the mid-dorsal region, but under the microscope a few 
myelinated fibres could be seen ; there was considerable destruction 
of the cord up to the level of the fifth cervical root, above which 
there were the usual ascending degenerations ; below the level of 
the lesion there was considerable myelitis, giving rise to destruc- 
tion of the peripheral portion of the cord. May 2nd, 1899. 

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9. Further evidence on the pathology of diphtheritic paralysis. 

By Fbbdebice E. Batten, M.D. 

[With Plate II.] 

WHILE examining pathologically certain cases of diphtheritic 
paralysis, the results of which were read before the British 
Medical Association in July, 1898, and were published in the 
* British Medical Journal ' under the title of '* The Pathology of 
Diphtherial Paralysis,'* ^ I was struck by the fact that although 
the pathological change found in the nerves was definite and 
marked in nearly all cases of long standing, yet in one case, a child 
aged four years, in whom the disease had existed fifty days, no. 
change could be demonstrated in the nerves. I determined, there- 
fore, to continue to examine pathologically all cases of diphtheritic 
paralysis that I could obtain, and since that date I have, thanks to 
the kindness of Dr. Bastian, Sir Dyce Duckworth, Dr. Hensley, 
and Dr. Penrose, been able to examine five cases. 

Method of examination, — The same methods have been used as 
in the previous series of cases, viz. Nissl's method, Marchi*s method, 
and Pal's method, but in addition to these the nerves have been 
examined by Stroebe's method for staining axis-cylinders. 

Nature of changes found : 

NissVs method. — Three of the cases were examined by this method ; 
in one case (No. 3) all the cells of the anterior horn appeared per- 
fectly normal ; in the second case (No. 1) only one abnormal cell 
could be foimd in the cervical region, the cell having become 
swollen, the nucleus eccentric, the chromophilic substance displaced 
to the periphery, and the protoplasm of the cell finely granular 
(fig. 1) ; all the other cells stained normally and well. In case 
No. 2 there were some very definite alterations in the cells of the 
anterior horn, the cells being shrunken, pigmented, the chromo- 
philic substances staining badly, and the processes of the ceU 
indistinct ; the nucleus, however, in most of the cells had not 
become eccentric ; the changes, therefore, are for the most part not 
in the Nissl bodies, but rather in the shape and pigmentation of 
the cell. Pigmentation of the cell has little pathological signifi- 

1 * Brit Med. Journ.,' November 19th, 1898. 

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Illustrating Dr. Frederick E. Batten's paper *• On the Pathology 
of Diphtheritic Paralysis." (Page 22.) 

Fig. 1. — Cells of the anterior horn at tlie level of the fifth cervical root from 
a case of diphtheritic paralysis, in which death occurred od the fifty-eighth day 
of the disease. Foar cells are shown: three are of normal appearance; the 
foarth is seen to be swollen, globular in shape, the chromophilic material 
lying to the periphery, while the cell body is finely granular, with an indistinct 
nucleus becoming eccentric in position, and tending to become extruded from the 
cell. No change can be seen in the nucleolus. 

Stained by Nissl's method. 

Fig. 2. — Longitudinal section through the left phrenic nerve of the same case 
to show the characteristic changes which take place in the myelin sheath. It 
will be seen that only certain of the fibres are aflPected ; the sheath of the nerve 
is somewhat swollen, and occupied by fine black granules in parts. Wbere the 
degeneration is more advanced these fine granules have passed into larger fat 

Stained by Marchi's method. 

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' ' ) 

>]' / •.■■If], i .^ i tj,<- ' t-\- '* 'I*... Uy 
««■ 1 '*•. ' I •■• ..r lu.nnul :ip \'it •■»' «' ; t"'; ' 

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. .. ll *■ '.iv'-'i.i >!:. ,iiM. It 
'1: rKc .1' atli -f M..' '.TV,. 
l^^'\U 8 !*i T),i ti, \\\,c! • i t 

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Path. Soc. Trans. Vol. L. Pl. II. 


,r"^ -^-'^ • -^ 

J» ,KiT.#iiiii^ 

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fig. t 


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caDce» inasmucli as it is always present in the cells of old persons ; 
and with regard to the other changes it must be borne in mind 
that the cord was remoTed from the body of a patient, who died of 
septic pneumonia, some thirty hours after death. 

With regard to the condition of the cell my attention has been 
called to a very interesting paper published by Dr. Sharkey ^ in 
'Brain/ 1890, on a case of diphtheritic paralysis, in which he 
figures the nerve-cells of the anterior horn stained by logwood. 
The cells as figured resemble a perfectly healthy cell as stained by 
Nissl's method. No lesion was found in any other portion of the 
body, and it is suggested that the changes observed in the motor 
cells were the result of the diphtheria poison. 

Ma/rchVs method, — The characteristic changes (Fig. 2), vijs. the 
swelling of the myelin sheath with deposit of fat globules, and later 
the breaking up into oval masses, which I have recently described, 
were found in the nerves, anterior and posterior nerve-roots of all 
the cases except No. 3, in which no change could be found, and in 
which the changes in the cells of the anterior horn above described 
were found. The changes were not limited to the nerves of the 
trunk, but affected also certain of the cranial nerves, being most 
marked in the third, fourth, and sixth, and in that portion of the 
fifth that contains the large fibres ; the optic and the auditory 
nerve I have never found affected. The amount of change in the 
parts examined varies to a very considerable degree, in one case 
the peripheral nerves, in another the anterior roots, in another the 
posterior being most affected. 

FaVa method.— "By this method the nerves appear to be perfectly 

Stroebe's method, — By this method the axis-cylinders have been 
stained ; so far as can be seen no change has taken place in them, 
but as an osmic acid preparation of the nerve will not stain satis- 
factorily by Stroebe's method, it is difficult to say whether there 
may not be some affection of the axis-cylinder at a point where 
alteration of the myelin sheath has taken place. 

Conclusions. — Five cases have been examined ; four of these ex- 
hibit the characteristic changes in the nerves or roots, while in only 
one were these absent. Changes in the anterior horn cells have been 
noted in two cases ; in one of these, however, only a single altered 
cell was found, and in the other the cause of death and the interval 
I ' Brain,' vol. xiii, p. 237, 1890. 

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between death and post-martem is too great to allow one to accept 
this case without hesitation, and I can only repeat the conclusion 
of my former paper, yiz. that the dominant lesion in diphtheritic 
paralysis is a parenchymatous degeneration of the myelin sheath 
or the nerves, although one must always be prepared to find a 
certain proportion of cases which give a negative result. It seems 
almost certain that a general poison like that of diphtheria must 
act on the whole neuron, and what I have endeavoured to show is 
that the effect of the poison manifests itself (at least in fatal 
cases) in the myelin sheath and not in the cell body. 


Oases. — 1. Girl aged 11 months, duration of disease fifty-eight 
days. 2. Woman aged 28 years, eighty days. 3. Boy aged 4 years, 
forty days. 4. Boy aged 2f years, uncertain. 5. Girl aged 5 years, 
forty-five days. 

Parts examined, — Cranial nerves, spinal cord, anterior and pos- 
terior nerve-roots, vagus and phrenic, nerves to the upper extremity, 
nerves to the lower extremity. 

Methods of examinaiion. — 1. NissFs method ; 2. Marchi's method ; 
8. Pal's method ; 4. Stroebe's method. 

^Casb 1. — ^D. Or — , aged 11 months, was admitted to St. Bar- 
tholomew's Hospital, under the care of Dr. Hensley, to whom I am 
indebted for the notes of the case. She was taken ill six weeks 
previously with croup and bronchitis, she had difficulty in breath- 
ing for fourteen days, and had not been quite well since. Three 
weeks later the child began to have regurgitation of fluid through 
the nose. On admission the child had a feeble cry, the diaphragm 
acted very badly, and on attempting to drink milk regurgitated 
through the nose, the soft palate was paralysed, and the limbs 
were flaccid and wanting in tone. The knee-jerks were absent. 
Urine contained a trace of albumen. The child lived for sixteen 
days after admission to the hospital, and then died suddenly. At 
the autopsy some collapse and broncho-pneumonia of the lungs 
were found, the other organs appearing normal. 

Pathological examination, — (1) Nissl's method. Only one ab- 
normal cell could be found by this method in the cervical region, 
all the other cells appearing normal (fig. 1). 

(2) Marchi's method. Cranial nerves: degeneration in the 

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third, fourth, fifth, and sixth nerves was found to a variable ex- 
tent. Spinal cord: no change could be found. Spinal roots: 
changes were present in the anterior and posterior roots, but were 
more marked in the anterior than in the posterior, and in the 
cervical than in other regions of the cord. Peripheral nerves: 
changes were present in the va^i, phrenics, the anterior crural 
nerves, and in the brachial plexus, the changes being most marked 
in the phrenics (fig. 2). 

(3) Pal's method. By this method all the parts above examined 
appeared normal, or the changes were so slight that no patho- 
logical significance could be attached to them. 

(4) Stroebe's method. No alteration in the axis-cylinders could 
be demonstrated by this method. 

Case 2. — M. J — , aged 28 years, was admitted to St. George's 
Hospital, under the care of Br. Penrose, to whom I am indebted for 
the notes of the case. The history of the case was as follows : — Six 
weeks previous to admission she had diphtheria, and was in bed 
for fourteen days. About ten days later she noticed weakness in the 
feet and legs; this disappeared, but soon after the patient became 
hoarse and unable to swallow, fluid regurgitating through the nose. 
Weakness of her legs again occuiTed, and the right arm also 
became affected. Her eyesight was also affected for a short time. 

On admission, September 19th, 1898, no marked paralysis was 
present, there was some loss of sensation in the extremities, and 
the knee-jerks were absent. 

September 25th. — Tlie diaphragm and intercostals were partially 
paralysed, regurgitation of food had taken place throucjh the nose, 
and there was more dyspnoea. During the next month, although the 
condition of the diaphragm improved, the patient developed signs 
of bronchitis and pneumonia, and died on October 27th of septic 
pneumonia, an abscess cavity being found in the right lung. 

Pathological examincdion, — (1) Nissl's method. By this method 
considerable change could be seen in the cells of the anterior horn ; 
the cells were for the most part shrunken, the chromophilic sub- 
stance was altered, and there was a very considerable amount of 
pigment in the cell, but the nucleus was, as a rule, centrally placed 
in the cell, though it was by no means always well stained. The 
changes are rather more marked in the cervical than in the lumbar 

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(2) Marchi's method. By this method no change conld be 
demonstrated either in the cord, anterior or posterior roots, or 
in the peripheral nerves. 

(3) Pal's method. No change could be demonstrated in the 
parts examined bj this method. 

(4) Stroebe's method. The root-fibres and the peripheral nerves 
examined bj this method appeared perfectly normal. 

Case 3. — E. G^— , aged 4, was admitted to St. George's Hospital 
under the care of Br. Penrose, to whom I am indebted for the 
notes of the case. 

The child was admitted on September 17th, 1898, with the 
history of having had a sore throat for two days ; tracheotomy was 
performed, and the child progressed favourably and was apparently 
well on October 11th. A few days later regurgitation of fluii 
through the nose was noticed, bronchitis developed, and the child 
becoming gradually weaker, died on October 24th. 

Pathological examination, — (1) Nissl's method. The cells of the 
anterior horn appeared to be perfectly normal. 

(2) Marchi's method. Spinal cord : no change could be found 
in the spinal cord by this method. Spinal roots : the characteristic 
changes were fairly marked in the cervical and lumbar regions of 
both the anterior and posterior roots ; in the dorsal region the 
changes were less marked. The peripheral nerves of this case were 
not preserved. 

. Case 4. — M. S — , aged 2| years, was admitted to St. Bartholo- 
mew's Hospital, under the care of SirDyce Duckworth, to whom I 
am indebted for the notes of the case. The onset of his illness was 
indefinite, as he had not been well since measles, six months pre- 
viously. On June 27th, however, he suddenly lost power in his legs ; 
on July 4th, fluid regurgitated through the nose. 

• On admission his legs were flaccid, his diaphragm was acting 
very feebly, and his knee-jerks were absent. Ho had several 
attacks of dyspnoea. He died on July 9th. The autopsy showed 
some broncho-pneumonia and deposit of tubercle in the right 

Pathological examination, — The nerves only were examined in 
this case; the anterior tibial and the vagus showed change to 

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a moderate degree, while the cliatiges in the phrenic were very 

Case 6. — M. P — , aged 6 years, was admitted to the National 
Hospital under the care of Dr. Bastian, to whom I am indebted for 
the notes of the case, with the history that she had been well till 
seven weeks previously, when she had a bad throat lasting about 
three weeks, and had been veiy weak ever since. During the last 
two weeks she had had difficulty in swallowing and had had some 
regurgitation of fluid, and her articulation had been thick and in- 
distinct. On admission the voice was nasal, pupils were dilated 
and reacted badly to light, together with slight double ptosis. The 
legs were flaccid and the knee-jerks absent ; the diaphi-agm acted 
feebly. The child died three days after admission. 

Pathological examination. — (1) Nissl's method. Omitted. 

(2) Marchi's method. Spinal cord: no alteration could be 
found. Spinal roots : changes are present to a very slight degree 
in both the anterior and posterior. Peripheral nerves: changes 
were present in the anterior crural, vagus, and phrenic nerves, but 
were much more marked in the phrenic than in the other two. 

(3) Pal's method. By this method the cord, roots, and 
peripheral nerves appeared to be perfectly normal. 

(4) Stroebe's method. By this method the axis-cylinders 
appeared normal. May 2nd, 1899. 

10. Neuroma of brachial plexus, with moUuscum fibrosum 

of skin. 

By T. Cabwabdine, M.S. 

OC — , aged 25, was seen in consultation for a tumour at th« 
• root of the neck on the left side, about the size of a duck's 
egg, nodular, moveable, tender, and non-adherent to the skin. It 
extended deeply under the sterno-mastoid and clavicle. It was 
first noticed three or four months before, and had gradually grown 
so as to become painful and inconvenient. About seven weeks 
previously the patient had what he called a strain at the heart, 
temporarily followed by sharp pains in the chest. 

All over the body, but chiefly about the trunk, he had numerous 

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nodules, many with comedones and minnte venules upon them, 
some discoid and subcutaneous and some peduncidated. Thej 

Fio. 6. 

Nearoma of brachial plexus with moUuscum fibrosum. 

varied in size from that of a hemp seed to a hazel nut. Upon the 
right buttock was a large pendulous fibroma. Several large, 
brownish, pigmented patches of irregular oval form and sharp 
outline were present about the trunk,i and there was a general 
dusky appearance of the whole skin resembling that of early 
Addison's disease, besides a multitude of small brown freckles. 

There were nodules on the skin as long as the patient could 
remember. In the usual glandular regions, and simulating en- 
larged glands very closely, were deeply-seated nodules, which were 
probably neuromata, particularly in the apices of both axillse, in 
the groins, and about two inches above the right internal 

The cervical tumour was exposed by operation, and when isolated 
proved to have deep attachments to the spine above and beneath 
the clavicle below. A longitudinal incision was therefore made, 
1 See Wickham, • Brit. Joum. of Dermatology,' 1890, p. 151. 

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and the tumour enucleated from what proved to be the outer cord 
of the brachial plexus, the fibres of which were expanded over the 
tumour, in parts very thinly so. The wound healed well ; there 
was no anaesthesia, but slight transient paresis of the deltoid 

On microscopical examination the neuroma presented the usual 
appearance of a soft cellular fibroma. 

The family history is thus represented : 

Father + 

I /o 

No sisters^Mother + — 3 brother*^ + 

/\ ^+ 

One daughter o One son + 
(The mark + signifies those affected with raolluscum flbrosum.) 


1. Atkinson. — * New York Med. Joum./ December, 1875. 

2. Von fiechUnghausen, — 'Ueber die Multiplen Fibrome der Hant/ Berlin^ 

8. Fayn€,-^' Path. Soc. Trans./ vol. xxxviii, p. 69 (two plates) ; also * Clin. 

Trans./ toI. xxii, 1889, p. 189. 
4. Smith (quoted by Payne). — ' Treatise on Pathology, &c., of Neuroma/ Dublin, 


The references to uncomplicated moUuscum flbrosum in the ' Pathological 
Society's Transactions' and elsewhere are numerous, and many are quoted in 
Crocker's * Diseases of the Skin,' London, 1893, p. 587. 

Jarmary llth, 1899. 

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1. Case of ulcer of the trachea, involving the left recurrent 
laryngeal nerve, and perforating into the aorta. {Card 

By NoEMAN Dalton, M.D. 

A MAN, aged 35, brought into King's College Hospital dead from 
haemoptysis. In the wall of the trachea, on the left side, 
about one inch above the bifurcation, there was an oval hole about 
the size of an almond. The edges were smooth and a little thick* 
especially at the upper end. The cartilages had completely dis*- 
appeared at this opening, and it led into a small cavity with 
irregular walls. 

The aorta was atheromatous. At a point just below the orifice 
of the innominate artery and on the right side of the tube there 
was a portion of the aortic wall, about the area of a sixpenny piece, 
which was very thin, and bad a slight aneurysmal bulge outwards. 
This was not, however, a true aneurysm, but a bulge formed by 
weakening of the outer wall of the aorta at that spot, because part 
of the floor of the ulcer in the trachea was situated just outside 
the bulge, and was thus undermining it. A small perforation was 
found between the ulcer and the aorta, and this was the cause of 
the fatal haemorrhage. 

Although no scar was found on the penis, the tracheal ulcer was 
probably syphilitic. The tongue looked syphilitic, and in other 
parts of the mucous membrane of the trachea there were small, 
slightly raised patches like syphilitic plaques. Microscopically one 
of these plaques was found to consist of three mucous glands, not 
distended by mucus, but with the walls of their acini infiltrated 
by leucocytes to such an extent that the acini were compressed. 
There was, in fact, a subacute interstitial inflammation of the 

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gland. The central part of the plaque (both gland-tissue and 
leucocytes) was necrotic. The tissues around the plaque were also 
infiltrated with leucocytes. Over the plaque the epithelium was 
practically absent, but to the naked eye it did not look like an 

One of the patient's friends said that the dead man had been 
undergoing treatment for paralysis of the larynx, and the left 
recurrent laryngeal nerve could be traced as far as the outer wall 
of the tracheal ulcer, where it became lost. March 21«<, 1899. 

2. A case of pressure on the recurrent laryngeal nerves by calca- 
reous glandsy with anthracosis of the lungs. {Card specimen.) 

By NoBMAN Dalton, M.D. 

THE patient, a man aged 73, a clay pipe maker, was under treat- 
ment for paralysis of the left recurrent laryngeal nerve. 
The right recurrent became affected also, and tracheotomy was 
performed, but death followed soon after. 

Between the arch of the aorta and the trachea there was a dense 
fibro-calcareous mass. It was partly composed of lymphatic glands, 
which were calcareous and black. Into this mass the left recur- 
rent laryngeal nerve entered, but it could not be traced through 
the gland. On the right side of the trachea numerous smaller 
calcareous glands were found, and in one of these the right recur- 
rent laryngeal was involved. 

In both lungs there were large solid areas, which were very hard 
and quite black. In some of these areas there were cavities with 
rough walls, like tuberculous cavities. Inside the cavities there was 
an opaque, muddy-looking black fluid, which had no gangrenous 
odour. It looked like a mixture of finely-divided carbon and thin 
mucus. Microscopically no tubercles were found in the lung. 

The man had never been a miner, and the question arose as to 
whether the anthracosis of the lungs and the calcification of the 
glands could have been due to his occupation, that of making clay 
pipes. I inquired of his widow, who told me that he only worked 
in wet clay, from which he could inhale no particles, but that he 

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complained much of the dust in the work-room, especially when 
the room was swept. She also said that his clothes were always 
covered by dust. He also seems to have complained of a smell of 
sulphur when the pipes were baked. 

Mr. Herbert Jackson, the senior demonstrator of chemistry in 
King's College, Loodon, was so good as to analyse the glands for 
me. He says that the black matter is undoubtedly carbon. The 
question of sulphur led him to examine particularly for iron, and 
he says that iron will only account for one-tenth of the blackness. 
He found that the calcareous matter consisted of 50 per cent, of 
calcium carbonate, and that the remainder was made up of alumina 
and silicate of alumina. He thinks that this large amount of 
alumina and silica indicates that the particles in the glands were 
derived from the clay with which the man worked. As he was 
seventy-three years old, he had plenty of time in which to absorb 
such large quantities. March 2\8t, 1899. 

8. Transverse fracture of the cartilaginov^ portion of the 
trachea. [Card specimen,) 

By W. S. Lazabus-Bablow, M.D. 

THE specimen was taken from the body of a man aged 73, who 
was the subject of the following accident : — While looking 
down the well of a lift the car descended from above, forced his 
head downwards against his thorax, and over the rail over which he 
was looking. The patient was veiry collapsed when admitted into 
hospital, but nevertheless lived thirteen days, ultimately dying 
with hypostatic pneumonia. At the autopsy it was found that 
there was a fracture of the sternum at the junction of the manu- 
brium with gladiolus, a fracture of the third right rib, separation 
of the second and third libs from their respective cartilages, and 
the fracture of the trachea now shown. The cartilaginous portion 
of the trachea 2i inches below the rima glottidis is the seat of a 
clean fracture which passes between two contiguous lings, and 
extends backwards to the muscular portion, which was unaffected. 
The soft tissues in the neighbourhood gave little or no evidence of 

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the injury. There was a remarkable absence of atheroma or cal- 
careous change throughout the body. 

The only case in the Society's * Transactions * in any way 
comparable with this was communicated by Mr. Oodlee (vol. xxvi, 
p. 18, 1875). It was in a child aged seven years, was longitudinal, 
involved both anterior and posterior sui*faces of the trachea, caused 
separation of the right bronchus from the rest of the trachea, and 
was also the result of an accident, the child having been run over. 
In Holmes's ' System of Surgery ' three cases of fracture of the 
trachea are recorded, one of which ended in recovery. 

March 7th, 1899. 

4. Case of hypertrophy of the right lung with obliteration of 

the left. 

By Norman Dalton, M.D. 

THE patient was a man aged 45. No past history of the case 
was obtained as the man was dying of pneumonia when 
admitted into King's College Hospital under Dr. Cumow. 

At the post-mortem no external deformity of the chest was 
noticed. On removing the sternum the right lung was seen cover- 
ing the whole of the front of the chest. After filling the anterior 

Pig. 7. 

Fig. 8. 

YiQ, 7, — Diagrammatic representation of hypertropbied right lung, anterior 
aspect, a. Upper lobe. h. Lower lobe. o. Middle lobe, d. Heart. 0. Adhe- 
sions. /. Diaphragm. 

YiQ, 8. — Diagrammatic representation of hypertrophied right lung, posterior 
aspect. A. Bight Inng. B. Left lung collapsed. 0. Heart, a. Aorta, h. Left 
bronchus, e. Diaphragm. 


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mediastinum it ascended into and quite filled the left subclavicular 
area, when it was covered by its own pleura. So complete was 
this substitution of right lung for the apex of the left lung, that it 
is probable that in health the physical signs at the left apex were 

Below the subclavicular area the right lung occupied the left 
mammary and the precordial areas. 

The heart occupied the left axillary region, only a small part of 
the left ventricle being uncovered by the right lung. The left lung 
was shrivelled and occupied the lower two thirds of the left 
vertebral groove behind. 

On further examination it was found that the lower lobe of the 
right lung was pneumonic, and that the pleura over it was 
obliterated by old adhesions. The hypertrophy was due to 
enlargement of the front part of the upper and middle lobes. 
The extreme left border of the hypertrophied parts was emphyse- 
matous, and there were one or two old adhesions, notably one to 
the first left rib, which anchored what I may call the left apex of 
the right lung, and a large one which bound the lowest part of 
the hypertrophied middle lobe to that part of the diaphi-agm where 
the pericardium is usually situated. 

The left lung was rather longer than the lung of a foetus at full 
time, but quite flat and airless. The bifurcation of the trachea 
was normal, but the left bronchus was the smaller, and became 
further narrowed at about one inch from its origin. This narrow- 
ing appeared to be due to pressure on the bronchus from above, 
because, while the lower side of the tube was fairly straight, the 
upper side was concave on the outside and projected into the 
lumen, making the stricture. This concavity was just at the spot 
where the aorta crosses the bronchus, but the vessel was quite 
clear of the tube and could not have compressed it. I expected to 
find some enlarged glands here, but those I found were only 
slightly large from recent inflammation, and, while in search of 
something more definite, I removed them as you see in the specimen. 

Above the stricture the bifurcation of the bronchus was found, 
and here the tube was larger again. After the bifurcation the 
branch to the lower lobe of the lung quickly became too small to 
follow, but that to the upper tube remained perceptible for another 
inch, but was curiously twisted, and its wall was thick and cal- 

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As regards the heart, there was slight acute pericarditis, with 
moderate effusion, but this could not have compressed the left 
lung, because the inflammation was quite recent, the pericardium 
showing no old thickening. The heart, as a whole, was large, 
possibly because it helped to fill up space, but the greater enlarge- 
ment of the right ventricle, which formed the apex of the whole 
viseus, indicates that the hypertrophy of the right lung did not 
produce complete functional compensation. 

Memarhs, — The cause of the collapse could not have been direct 
pressure on the lung, because there was no tumour or effusion or 
trace of old effusion in the thorax capable of causing such 
pressure. It must therefore have been due to obstniction of the 
left bronchus, and we find evidence of this in the distortion of the 
main bronchus and its upper branch. 

As regards the nature of the obstruction, if the distortion of the 
tube were congenital, I do not think that the lung would have 
grown to its present length while it contained no air and did no 
work. There is no sign of a foreign body in the tube, and I 
cannot think of any lesiOn, beginning in the mucous membrane, 
which would be likely to cause such distortion. It is therefore 
probable that the obstruction was due to pressure on the tube from 
without, and this view is supported by the depression of the upper 
wall of the left bronchus. In addition the aorta is separated from 
the bronchus by a considerable space, which before dissection was 
occupied by glands, and if the finger is put into the aorta, an ^ngle 
can be felt instead of a gradual curve. I think, therefore, that at 
an early period of life there must have been a mass of enlarged 
glands between the bronchus and the aorta, and that these, after 
compressing the bronchus until complete collapse with obliteration 
of the air vesicles occurred, became smaller again. The pressure 
must have been gradual to allow hypertrophy of the right lung to 
occur instead of mere emphysema. In favour of the view that the 
pressure was partly removed after the mischief was done is the fact 
that the bronchus looks as if it must have at one time been smaller 
than it is now, for with its present lumen complete collapse of 
the lung could scarcely occur. 

The specimen shows the difficulty that the lung has in becoming 
hypertrophied. One kidney or one testicle can hypertrophy as much 
as is necessary when its fellow is destroyed, for they have only 
increase of function to perform. But the lung has to enlarge not 

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onlj to perform increased function, but to fill up space. To 
accomplish the last object both the old and the new air vesicles 
become stretched and finally emphysematous, so that much of the 
new tissue is useless for the purpose of respiration. The large size 
of the right ventricle in this case shows that the one lung was, 
although so large, not performing fully the function of the 
two. October 18^, 1898. 

5. Lung showing uniformly distributed fibrosis, 
(Card specimen.) 

By A. E. Gareod, M.D. 

PART of the right lung of a man, aged 89 a carman, who was 
not known to have followed any ** dusty occupation." He 
died of cardiac failure with anasarca and dyspnoea. The heart 
was hypertrophied and generally dilated. In the ventricles were 
^nte^mortem clots. 

Both lungs were bulky, tough to the knife, and of nearly double 
the normal weight. The upper lobe of the lung shown exhibits 
emphysematous bullcB. There were some pleuritic adhesions, but 
the pleura is not thickened. The lung tissue is everywhere in- 
tersected by bands of bluish-grey fibrous tissue, forming a fine 
meshwork which contrasts strongly with the reddish tint of the 
congested lung. The nodes of the meshwork stand out as grey 
granulations, but there is no tubercle anywhere. The bronchi are 
neither dilated nor thickened. The bronchial glands were not 

Under the microscope the lung shows diffuse infiltration with 
fully -formed connective tissue. Small inflammatory foci, composed 
of round cells, are found here and there, but nothing suggests 
tubercle. There is not more pigment than is usually present in 
the lungs of town dwellers. May 16th, 1899. 

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6. A case of sarcoma of Itfl lung and mediastinum. 
Bj Chablis D. Gebbn, M.D., F.R.C.S. 

THB patient was a girl, aged 14 years, who was under obserration 
for some three months before her death, complaining of 
general weakness and djspnoea on actire exertion. She was said 
to have been always rather delicate, and to have had attacks of 
pain in back and limbs attributed to influenza, but she had not 
been laid up for any length of time, and no date could be assigned 
for the commencement of the symptoms. There was no history of 
malignant disease in the family. When first seen on May 20th, 1898, 
there was dulness on percussion over the whole left side of the 
ehest both anteriorly and posteriorly, with total absence of breath- 
sounds, except over a small area in the first intercostal space near 
the sternum, where a faint tubular breath-sound could be heard. 
The resonance over the right lung was normal, and at that time 
certainly extended well to the left border of the sternum. There 
was normal vesicular breath-sound over the whole of the right 
lung. The stomach resonance reached as high as the fifth rib. 
The cardiac dulness could not be distinguished as a separate area, 
but was not extended to the right side beyond its normal limit. 
The apex-beat could just be felt in the fifth space within the nipple 
line, but was very feeble. There was a soft systolic murmur 
audible with every beat. The left side of the chest scarcely moved 
with respiration, and was obviously contracted as compared with 
the right. There were no enlarged superficial veins over the front 
of the chest, and no enlarged cervical glands. I could detect 
nothing abnormal in the abdomen. 

She was a bright and intelligent girl, and had attained the 
physical development normal to her age ; she was not anaemic, and, 
though not fat, showed no signs of recent loss of flesh. There 
was no pain nor stiffness in any of the joints. I thought the case 
was one of consolidation and contraction of the left lung, probably 
oonsequent upon antecedent pleural effusion, complicated with 
mitral regurgitation, and that the attacks of pain which had been 
described had probably been that form of acute rheumatism with 
little joint affection so frequently seen in children. I did not 

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think that there was at that time any fluid in the pleura, and 
refrained from inserting a needle. For some weeks no very 
obvious chaiUge took place, but she merely seemed to become 
gradually more feeble. On July 16th, on her return from a short 
visit, I noticed a small, hard gland just above the right clavicle, 
and there was then for the first time distinct stridor on deep 
inspiration, and a dilated, superficial vein could be seen runtnng 
obliquely across the manubrium sterni. Her general nutrition 
was obviously failing, and from this time she got worse with great 
rapidity, a gland appeared above the left clavicle, and in the course 
of a few days a large glandular mass had formed above both 
clavicles. The heart's action was much more feeble, and the 
expansion of the right lung less perfect ; the dyspnoea increased in 
severity, and emaciation attained an extreme degree with quite 
remarkable rapidity. The diagnosis of malignant disea^se in the 
lung and mediastinum was now easy enough. On July 22nd slight 
jaundice was for the first time noticed, and the gall-bladder could 
be felt. She was then, however, much too ill for detailed clinical 
examination. Death took place on July 23rd from the combined 
effects of dyspnoea and general nutritional failure. 

At the autopsy, made sixteen hours after death, the body was 
extremely emaciated and slightly but distinctly jaundiced. 

There was a mass of enlarged glands above each clavicle. On 
opening the thorax a large malignant mass was seen, which was 
found to extend from the sternum to the vertebree and from the 
xiphoid to the upper opening of the thorax ; it was adherent to, 
but had not eroded, the sternum ; it had commenced to erode the 
body of the second dorsal vertebra on its left side ; it had com- 
pressed the heart from above downwards, and had displaced the 
oesophagus somewhat to the right ; it did not appear, however, to 
have infiltrated its walls nor to have obstructed its lumen to any 
material extent. The arch of the aorta and the great vessels were 
completely embedded in the growth, as well as the upper part of 
the pericardium. 

There was general adhesion of the pericardium, the right ven- 
tricle was somewhat hypertrophied, no valvular disease was made 
out. The left pleura was universally adherent, and the lung was 
with difficulty removed with the mass ; on section the left lung was 
seen to have been converted into a malignant mass, which appeared 
to have grown from the hilum outwards, and which was surrounded. 

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except at the apex, by a narrow fringe of indui'ated and airless lung 
tissue. The right pleura was normal ; the right lung showed on 
section two small nodules of malignant new growth. 

The pancreas was, with the exception of a small portion near its 
tail, replaced by a mass of new growth, over which the first two 
portions of the duodenum were stretched, and which had 
obstructed the common bile-duct. The lymphatic glands around 
the pancreas were enlarged, but not those in the portal fissure. 
The gall-bladder was much distended. The liver showed two 
small nodules of new growth, and its capillaries were distended 
with dark green bile. 

There was a small spot of recent inflammation on the mesentery 
near the pancreatic growth, but the peritoneum was otherwise 

Spleen, kidneys, and intestines normal. Uterus and appendages 
normal. Brain not examined. 

The growths were white on section, of firm consistence, and in 
the older portions of the larger masses showed bands of fibrous 
tissue. In the centre of the pancreatic growth was a small cavity 
with fluid, milky- white contents. On microscopical examination the 
growth was found t>o be a sarcoma with round, fusiform, and oval 
cells, and a relatively small amount of fibrous tissue. In sections 
taken from outlying portions of the growth groups of sarcoma cells 
could be seen extending along the walls of the blood-vessels. 

In the mediastinal tumour, both in front and behind, the out- 
lines of individual glands could still be distinguished. 

Preparations of the mediastinal tumour with the heart and 
portions of the lungs attached, and of the pancreas and liver with 
microscopical sections showing the characters above described, 
were exhibited. 

I think the growth was certainly primary in the thorax, and I 
am inclined to think that it began in the glands at the hilum of 
the left lung and invaded the lung first and then the mediastinum, 
and that the other growths were later secondary deposits. The 
massive character of the growth in the left lung contrasting with 
the nodular deposits in the right lung, the firm fibrous bands in 
its centre, and the general uniformity of the rest of the mass, 
together with the fact that the clinical evidence of loss of function 
of the left lung was an early feature in the case, are, I think, in 
favour of this view. 

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The rapid failure of nutrition was, I think, due to the destruc- 
tion of the pancreas. In 1891, at this Society, Dr. RoUeston showed 
specimens from a case in which the distribution of malignant 
growths was very similar to that in this case, in which no 
symptoms were attributed to the growth in the pancreas, but the 
head of the organ was not in that case affected and the function of 
the organ presumably not destroyed. In that case the growth was 
scirrhus, and described as primary in the pancreas. 

In the 'Archives de MMecine' for 1890 there is an interesting 
and instructive paper by LetuUe on mediastinal tumours originat- 
ing in the remains of the thymus, with details of eight cases, but 
the distribution of the lesions was in none of them quite similar to 
that in this case. The presence of a systolic murmur was a notable 
feature in some of the cases, and I have myself observed it in some 
other cases in which I have bad reason to believe that there was 
enlargement of mediastinal glands. 

Germain See, in his work 'Maladies sp^cifiques de Poumon,' 
quotes from Jaccoud a case in which in the space of eight or ten 
days a malignant growth had filled the whole of the upper part of 
the anterior mediastinum and had invaded the entire upper lobe of 
the right lung, but the grounds upon which this limitation of time 
is based are not stated. 

In the museum of the Royal College of Surgeons there is a speci- 
men. No. 2858a, which was shown by Dr. S. West at this Society 
in 1883, which was taken from a boy aged sixteen years, and in 
which there is a similar mediastinal tumour which has invaded the 
adherent left lung, and in which the great vessels are embedded. 
There does not appear to be in this specimen the same conversion 
of practically the entire lung into a malignant growth which exists 
in the specimen shown this evening. In the same collection there 
is another specimen showing the aorta embedded in a malignant 
growth. Both of these specimens are described as lympho-sarcoma. 

Deceviber 20th, 1898. 

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1. Dextrocardia; left superior vena cava ; endocarditis, 
{Card specimen.) 


BOY aged 15. During life the position of the heart was obviously 
on the right side of the chest. The liver was in its usual 
place. The spleen was very large. Death was due to embolism. 

Post-mortem, — The right lung had two lobes only. 

The apex of the heart was beneath the sixth right rib, 2^ inches 
from the middle line of the sternum. 

The pulmonary artery was more exposed than usual, and its 
course before bifurcation was longer than usual. 

The superior vena cava was noi-mal, though small. On the left 
side a vessel as large as the superior vena cava ran straight down 
from the left jugular vein until it reached the left auricle. There 
it entered the coronary sinus behind the left auricle. The coronary 
sinus was very large, and entered the right auricle by an opening 
which just admitted the forefinger. This was practically a per- 
sistent left duct of Cuvier. 

The left innominate vein was represented by a very small vessel. 

There were f ungating vegetations on the mitral valve. 

November 1st, 1898. 

2. On dilatation of the right ventricle upwards and to the left. 
By T. Stacet Wilson, M.D.Edin., M.E.C.R 

niHE aim of this paper is twofold : — Firstly, to demon«trate the 
J- change in shape which the upper part of tlie right ventricle 
undergoes when it dilates ; and secondly, to show the changes 
in the pulmonary artery which result from this upward dilatation 
of the right ventricle, and point out the bearings which they 

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have upon the causation of the systolic murmur which is heai*d 
over the pulmonary artery in cases of cardiac overstrain and 
anaemic dilatation of the heart. 

Fio. 9. 

No. 1. 

No. 2. 

No. 3. 

Photograph of cardiac veutricles from above after removal of the aorta, 
pulmonary artery, and the two aaricles. No. 1. Normal heart. It will be 
noticed that little of the anterior wall can be seen, and that the base of the 
pulmonary artery is in the photojcraph almost vertically over the aortic valves. 
No. 2. Heart with slightly dilated right ventricle. It shows that the anterior 
wall of the right ventricle bulges forward in front of the aorta, and pnshes 
the origin 'of the pulmonary artery to the left of its normal position. No. 3. 
Heart from aortic and mitral disease, with dilatation and hypertrophy of 
both left and right ventricles. It shows very marked forward bulging of the 
anterior wall of the right ventricle and the considerable displacement of the 
pulmonary artery to the left. It also shows that the pulmonary valves and 
upper part of the right ventricle are not in the plane of the auriculo- ventricular 
septum as in hearts 1 and 2, but lie in a higher plane, ». e, are in the photograph 
projecting forwards towards the observer. 

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Fio. 10. 

No. 1. 

No. 2. 

No. 3. 

No8. 1 and 2. Lateral view of distended liearti, drawn from photographs, 
f natural size. No. 1. Normal heart. No. 2. Heart with slight dilatation 
of the right ventricle upwards. It shows the elevation of the pulmonary valves 
and consequent shortening of the artery, and also the altered direction of the 
artery relatively to the main axis of the right ventricle. No. 8. Semi-diagram- 
matic view of a normal heart as seen in section through the pulmonary artery 
and right ventricle. To illustrate the shortening and dilatation of the pulmonary 
artery which results from upward dilatation of the right ventricle. The dotted 
line represents the change that takes place. 

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This paper is illustrated bj the study of three hearts : 

1. From a man who died as the result of an accident. This 
heart may be considered normal. 

2. From a woman aged 48, who died suddenly from hemiplegia 
with cardiac failure, and who was found to have a congenital 
defect in the interauricular septum. In this case the right 
ventricle and right auricle are rather dilated, and the left are 
approximately normal. 

3. From a girl aged 15, who died from cardiac failure, the result 
of disease of both aortic and mitral valves. In this case the 
right ventricle is greatly dilated as well as the left ventricle and 

The hearts were distended with hard paraffin prior to their re- 
moval from the body, with the exception of No. 2, which was not 
distended in ntu. 

As to the pressure under which the injection was made, I em- 
ployed an ordinary injection syringe and did not use a manometer 
or other pressure gauge, but was careful not to over-distend the 
hearts. I cannot, therefore, state the pressure employed, nor do I 
consider it a point of importance in the present connection, since 
my object is to illustrate one of the ways in which the ventricle 
dilates, and not the degree of dilatation that occurs. I neverthe- 
less am confident that the specimens which I am showing are 
tmthful in this respect also. 

In addition to the casts of the entire heart I also show the 
ventricles isolated by the removal of the auricles and aorta and 
pulmonary artery. 

Comparison of the two dilated right ventricles thus isolated with 
that of the noimal heart shows very clearly the change in shape 
which takes place when the right ventricle dilates upwards in the 
manner so well described by Dr. Foxwell in his ' Essays on Heart 
and Lung Disease.' 

In a view of the isolated ventricles from al)Ove, as in the photo- 
graphs in Fig. 9, the dilated upper portion of the right ventricle 
is seen as a distinct prominence bulging forwards beyond the 
normal limits. Not only does it project anteriorly, as is well 
shown in the photographs of hearts 2 and 3, but it also projects 
upwards beyond the plane of the auriculo- ventricular septa, and so 
comes to overhang the commencement of the aorta. This is well 
shown in the case of heart No. 3, Fig. 10, wliere the isolated 

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ventricle is viewed from the side. It can also be seen in the 
photograph of heart No. 3 in Fig. 9. 

I do not show these specimens of upward dilatation of the right 
ventricle as an unusual condition, but as a good demonstration of 
a very common condition; for although this type of dilatation 
seems to be but seldom refeiTed to in current literature, I believe 
that if it be carefully looked for clinicallj and in the post-mortem 
room it will be found to be extremely frequent in cases of cardiac 
failure from a great variety of causes. 

It is, I believe, the ordinary type of dilatation in youth and 
early adult life, for at this period dilatation of the right ventricle 
upwards and to the left usually precedes and exceeds in amount 
any dilatation of the ventricle to the right. 

In adults this upward dilatation seems to be, as a rule, lees 
marked than dilatation to the right of the sternum, aod after the 
age of forty-five or so it seems to be decidedly rare, for in the later 
years of life the dilatation is towards the right side, and the conus 
arteriosus yields but little. 

This upward dilatation is often very extreme in youth and 
adolescence. For example, in Case 3 the relative dulness of the 
heart commenced above the second rib on the left side and 
extended to the nipple line in the third interspace, and after death 
some months subsequently the pulmonary valves were found to lie 
at the level of the first rib. Such a degree of dilatation is not very 

I now come to the consideration of the efiEect which this upward 
dilatation of the ventricle has upon the pulmonary artery. The 
effect of the upward extension of the conus arteriosus is twofold : 
firstly, the artery is shortened ; secondly, the direction of its course 
is altered. 

Firdly, as to the shortening of the pulmonary artery. It is 
evident that the increase of the upper part of the right ventricle 
upwards and to the left must carry the origin of the pulmonary 
upwards with it, and since the course of the artery is normally 
upwards from the pulmonary valves, any elevation of the point of 
origin must shorten the course of the artery. This is shown in 
Fig. 10 by comparing No. 1 with No. 2, and also in the dia- 

When, as is often the case, the pulmonary valves lie under the 
second rib instead of under the third, this shortening must amount 

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to I inch or more. Taking the normal length of the artery 
at 2^ inches, this would mean a shortening of 80 per cent. 
The effect of this shortening must be to relax the walls of the 

This relaxation may be seen post-mortem as a distinct wrinkling 
of the arterial wall in extreme cases. More often, however, the 
elastic contractility of the vessel prevents any distinct wrinkling. 
Although the relaxation of the vessel-wall may not show after 
death when the artery is empty, it cannot fail to cause some distor- 
tion during life. The relaxed wall is sure to yield abnormally to 
the blood pressure, and dilatation of the artery will result. There 
will, therefore, be both shortening and dilatation of the pulmonary 
artery, and the two combined will tend to make the artery become 
more spherical than normal. In other words, when the shortening 
is considerable there will be an aneurysmal bulging of the pul- 
monary artery under the influence of the blood pressure. 

And now as to the altered direction of the pulmonary artery. 
Taking the normal course of the first part of the artery as being 
obliquely upwards and backwards, it is evident that if its point of 
origin is raised its course will become more horizontal than normal. 
When, as often happens, the pulmonary valves lie under the 
second rib instead of under the third, the alteration in the course 
of the artery is considerable. 

This altered course means an alteration in the axis of the pul- 
monary artery as compared with the axis of the ventricle, and 
instead of the artery being fairly in line with the axis of the 
ventricle, as it ought to be, it will be at an angle to it. I have 
frequently noted this change in the direction of the pulmonary 
artery post m^ortem, more especially if the ventricle happened to be 
distended. Under such circumstances the sudden dipping back- 
wards of the artery is most noticeable. Thus, in the case of heart 
No. 3, 1 noted at the post-mortem that the first part of the pul- 
monary artery was at right angles to the longitudinal axis of the 
right ventricle, instead of being nearly in the same line as in a 
normal heart. 

In No. 3, Fig. 10, a semi-diagrammatic view is given of a section 
through the centre of the pulmonary artery and right ventricle to 
illustrate the distortion of the former. It is not easy to represent 
the change in the direction of the artery of which we are now 
speaking in this diagram, because it is accompanied by a move- 

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inent of the pulmonary artery and valves to the left of the normal 
position, t. 6. out of the plane of the diagram.^ 

This lateral movement of the artery is well shown in the photo- 
graphs of Fig. 9. In the normal heart, No. 1, the pulmonary 
valves are seen to be almost vertically over the aortic valves. In 
both of the other hearts the pulmonary valves and base of the 
pulmonary artery are seen to lie considerably to the left of their 
normal position. 

The practical result of this alteration in the direction of the 
pulmonary artery as compared with the axis of the ventricle, is as 
follows : — When the ventricle contracts the blood is thrown 
against the anterior wall of the pulmonary artery, instead of being 
thrown in the direction of its lumen. This will be seen on 
comparing No. 2 with No. 1 on Fig. 10. 

Here, then, we have two conditions eminently favourable to the 
production of an aneurysmal murmur. We have a pulmonary 
artery that becomes more globular than normal under the 
influence of the blood pressure, and we have the blood thrown 
into it so as to strike one of its walls — conditions likely to bring 
about a murmur-producing eddy in the dilated artery. 

These two factors, the increased distensibility of the pulmonary 
artery and the alteration of its axis, as compared with that of the 
right ventricle, are, I believe, of prime importance in the causa- 
tion of the common systolic murmur which is audible over the 
second left interspace in cases of cardiac overstrain and cardiac 
debility in anaemia and other diseases. 

In other words, I feel satisfied, from clinical and pathological 
evidence, to which I cannot refer within the limits of this paper, 
that the type of dilatation of the right ventricle with which this 
paper deals is the pathological condition which produces the 
common pulmonic systolic murmur of anaemia and overstrain, and 
that the mechanism is such as I have suggested. 

I do not say, however, that upward dilatation is sufficient by 

itself to produce this murmur in all states of the circulation, for I 

know that such is not the case. Extreme degrees of upward 

dilatation of the right ventricle can exist without producing any 

basal murmur. 

1 The attachment of the posterior part of the pulmonary artery and of the 
adjacent part of the right ventricle to the anterior part of the aorta and left 
ventricle is not sufficiently firm to prevent such a shifting of the pulmonary 
artery from taking place. 

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Upward dilatation of the ventricle gives rise to the possibility of 
an aneurysmal murmur being produced in the pulmonary artery. 

When the conditions of the circulation are favourable, an 
aneurysmal murmur is produced in the artery, and even an 
aneurysmal thrill. When they are not favourable no murmur is 
produced. When, for instance, the blood pressure in the pul- 
monary artery is high and the intra-tboracic pressure low, there 
will be a tendency for the artery to dilate easily, and remain more 
or less dilated, becoming practically an aneurysm. When, on the 
other hand, the intra-tboracic pressure is high, as in pneumonia, 
the external pressure on the artery will tend to hinder its dilata- 
tion, and it is not, therefore, surprising that in pneumonia extreme 
upward dilatation of the right ventricle can exist without any 
cardiac murmur being caused thereby. 

This, then, is the bearing which I believe upward dilatation 
of the right ventricle has upon the production of the pulmonic 
systolic murmur of anaemia and cardiac debility. 

AprU ISth, 1899. 

3. Extreme dilatation of the left auricle without mitral stenosis, 
[Card specimen) 

By H. MoRLEY Fletcher. 

THE heart, presented by T. H. Woodfield, Esq., to the Museum 
of St. Bartholomew's Hospital, was taken from a woman 
aged 47, who was under treatment at the Greenwich Infirmary for 
nearly five years previous to her death. During her life pre- 
systolic and systolic murmurs were heard at the apex. Cyanosis 
and much oedema were present. 

At i^Q post-mortem examination the left auricle was found dis- 
tended with recent clot. It was larger than the rest of the heart 
taken together. It measured seven inches in its transverse 
diameter, and five inches vertically. Its outer surface was 
injected and showed signs of fairly recent pericarditis. The wall 
was much thinned, and microscopically showed an almost com- 
plete absence of muscular fibres, the normal structure having been 
replaced by fibrous tissue, and containing calcareous plaques. 

The mitral orifice admitted three fingers. The mitral valve 

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segments were thickened. The left ventricle was dilated and 
hypertrophied. The right ventricle was also hjpertrophied. The 
lungs were highly emphysematous. 

Bemarks, — This extreme degree of dilatation of the left auricle 
is very unusual, and it was probably due, not to obstruction at the 
mitral orifice, but to the degeneration of the muscular tissue of its 
walls. It appears probable that this may have been secondary to 
pericarditis, the signs of which are visible over the auricle. 

November let, 1898. 

4. Spontaneous rupture of the heart. (Card specimen.) 
By Cecil F. Beadles. 

IN vols, xliv and xlvi of these ' Transactions/ cases of spontaneous 
rupture of the heart from insane persons have been recorded. 
To these are added two more. The heart shown weighs 15 ounces, 
and is in an exceedingly fatty state. In addition to much fat 
externally, the muscular wall has a pale, soft appearance from 
fatty infiltration and actual degeneration of the muscle-fibres. 
Small islands of fat can be seen embedded amongst the muscle. 
There are patches of thickening in the flaps of both the mitral 
and aortic valves. The aorta is very atheromatous ; the coronary 
arteries are obscured by the external fat, but the disease is seen to 
affect the orifices of these vessels. Two small rents exist on the 
anterior surface of the left ventricle about its centre. They are 
less than a quarter of an inch apart, and the longest is just a 
quarter of an inch in length. These open directly into the cavity 
of the left ventricle, but their inner extremity is concealed by the 
overhanging columned camese. 

On opening the pericardium a layer of dark clot was found com- 
pletely surrounding the heart, in front spread over as a thin film, 
but behind forming a great mass. The rupture occupied the 
centre of the exposed surface of the heart, and there was some 
blood-staining in the immediate vicinity. All the cardiac cavities 
were entirely free from fluid or clotted blood. Other organs were 
not examined. 

From male patient, 6363, aged 81, the subject of melancholia 


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for twentj-four years* He was an iDtellectual old man, who pre- 
viously had been a parish clerk, and who, during almost the whole 
period of his residence in Colney Hatch Asylum, made himself 
useful by assisting the medical staff with writing of a copying 
nature, at which he was most reliable and industrious, and wrote 
a neat and steady hand up to the last. He was subject to occa- 
sional periods of depression. For some years his heart was known 
to be in a weak and diseased state. Towards the close of last year 
he was several weeks in bed with geneml weakness, following an 
attack of acute gastritis, and from this he never regained his 
former strength, He, however, continued at his old employment 
up to the day preceding his death, although for some days he had 
more pain than usual over the cardiac region. Having done some 
writing in the morning of March 6th, he took a quiet walk in the 
grounds during the afternoon, and retired to rest at the usual time, 
having made no further mention of pain or uneasiness. At 4.30 
in the morning he was found dead in his bed, having been last seen 
alive at 2.30 a.m. It was obvious that he had passed away quietly 
within half an hour of being seen ; and another patient near, who 
had been awake during the interval, believed he had simply fallen 

The other case is one that occurred since my last communication, 
and differs from all the other hearts in the fact that the wall of the 
right ventricle gave way, and not the left. 

This heart was very fatty, and its wall could be readily torn near 
the junction of the ventricle and auricle of the right side ; a little 
lower was a rupture passing through the wall of the right ventricle. 
Aorta and other arteries atheromatous. Pericardium filled with 
clotted blood. Kidneys very granular, Liver fatty. 

From female, 5932, who died July 9th, 1895, at the age of 97,. 
having been insane thirty-two years. For many years she had 
been in a demented state, and for over ten years she had been sub- 
ject to chronic bronchitis and emphysema, with frequently swollen 
feet and legs. During the last five years she suffered from very 
feeble health and was almost blind. On June 8th she fell and 
sustained an intra-capsular fracture of the head of right femur. At 
the autopsy the fracture was found ununited and the capsule filled 
with fluid. Soon after a severe attack of diarrhoea set in, which 
lasted several days. The day before she died, not having been out 
of bed since the accident, she began crying out incessantly, but was 

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unconscious to all her surroundings. It is highly improbable that 
the heart received injury at the time of the accident, though it is 
just possible that a small branch of the coronary artery burst, and 
a clot forming in the wall of the ventricle finally caused the muscle 
tissue to give way. 

The last-mentioned case makes the tenth ruptured heart 
recorded in Colney Hatch Asylum in forty-eight years, during 
which period there have been 9290 deaths. It is worth noting 
that out of 10 cases of spontaneous rupture of the heart, in nine 
the rent occurred in the wall of the left ventricle. 

I will briefly add two cases of injury to the heart which come 
under a different category to the preceding. The first was 
probably rupture of a cardiac aneurysm, the second a case of 
bruising without actual rupture of the organ after external 

Male, 769, died suddenly in the year 1855, aged 33, after 
eighteen months' residence in the asylum, but the subject of 
epilepsy from childhood. A quantity of fluid blood and coagula 
existed in the pericardium, which had escaped from a rupture of 
a " morbid cyst on the apex of the right auricle." This case is 
said to have been published in the 'Pathological Journal,' Sep- 
tember, 1855. 

Male, 6611, a discharged soldier, addicted to intemperance and 
tobacco chewing, of violent and homicidal tendency, met his death 
in 1882, aged 28, after being six years in the asylum. He was 
struck several times on the chest with a shovel by a fellow patient. 
He fell at once and died immediately. The sternum was trans- 
versely fractured between the second and third ribs, and there was 
blood effusion into the soft structures. The pericardium contained 
about 2 oz. of straw-coloured fluid. The heart presented slight 
effusion of blood on the anterior surface of the left ventricle 
beneath the serous covering. All the cardiac cavities were quite 
empty, the muscle tissue slightly pale, valves normal, weight of 
organ 13^ oz. There was no rupture. Other organs in a normal 
state, with the exception of slight chronic changes in the brain and 
its membranes. March 21«^ 1899. 

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5. Heart thrombus in a case of enteric fever ; embolism of the 
right common iliac artery ; incipient gangrene of the leg ; 
multiple infarcts in the spleen and kidneys. 

By William Hunteb, M.D., F.R.C.P. 

THE specimens exhibited are: (1) thrombus in left ventricle; 
(2) large embolus impacted at origin of right common iliac 
artery, with distal portion of artery and its branches completely 
thrombosed; (3) corresponding veins, secondarily thrombosed; 
(4) recent infarcts in both kidneys, and in spleen. They are 
from a youth, aged 19, who was admitted into Charing Cross 
Hospital, under Dr. Green, on twelfth day of illness from typhoid 
fever, and who died on the twenty- third day. 

History, — Four days after admission (seventeenth of illness) he 
had a rigor, the temperature rising to KHG*', with sudden agonising 
pain about middle of right thigh on inner side ; and the right leg 
below knee became paler than left as far up as middle of thigh. 
Five hours later the limb was of a dead white colour, and cold up 
as far as knee, while above knee it was bluish and warm. Pulsa- 
tion could be felt in popliteal artery, but not in arteries of foot. 

By the following day (eighteenth) the condition of matters in the 
limb was such that the foot as far as a hand's breadth above ankle 
was of a dead white colour, and very cold ; the leg up to the knee 
was bluish, dusky, and very cold, with numerous ecchymoses ; the 
thigh bluish, cold to touch, and much swollen. No pulse could 
now be felt either in popliteal or femoral artery, and the groin 
was very tender. 

The limb was, uuder Mr. Boyd's directions, thoroughly shaved, 
washed, mercurialised, and wrapped in cyanide gauze and salicylic 
wool. The urine was smoky, although no blood could be detected, 
contained casts and granular dShris^ and large trace of albumen. 

During the following night (the nineteenth day) there was 
another rigor (temp. 104°, falling in four hours to 100*4^ and then 
rising in three hours to 105*8°), and his general condition was 
much worse. Pulse 130, heart- sounds very feeble. Resp. 44. 
Tongue dry and very fissured. 

The right /oo< was quite cold, yellow- white, beginning to shrivel. 

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Leg now almost uniformly bright red, ibis colour being 
unaffected bj pressure. 

Thigh bluish and swollen ; ecchymosed on inner side, blue on 
outer side. Sensibility to touch lost below knee, only slight above 

Next day (twentieth) sleeplessness and occasional delirium. Foot 
more shrivelled, leg somewhat swollen, thigh further swollen and 
more bluish. 

Twenty-first day and following day an irregular line of demarca- 
tion appeared about middle of thigh ; limb below this bluish red 
and cold ; above this dusky, swoUen, circulation in it very feeble. 

Death occurred on twenty-third day. During last three days 
temperature subnormal, varying between 96° and 98*^. 

Fo9Umortem (thirty hours after death). — Bight leg swollen and 
discoloured, a deep red livid colour from about the middle of thigh 
to lower third of leg. Foot and lower third of leg not discoloured ; 
toes shrivelled and dry. The upper limit of discoloration in thigh 
is sharply marked off from paler surface above by an irregular 
wavy border. Swelling most marked in upper thigh, and 
diminishes from above downwards. 

IntestineB showed limited typhoid lesions, ulceration, and pig- 
mentation in the lower three feet of ileum, chiefly in the lower 
foot. In caecum ulceration very deep down to the peritoneum; 
numerous ulcers in ascending and transverse colon. 

Heart weighed 9^ oz. Valves normal. Left ventricle moderately 
dilated ;. at extreme apex a polypoid thrombus adherent to its walU 
of a pale yellow colour, showing partial lamination ; centre partly 
softened. Thrombus measures one inch in length, three quarters 
of an inch in breadth. Microscopically is found to be made up of 
fibrin and leucocytes, with relatively little red clot. No clots or 
thrombi in left auricle. 

Common iliae artery, — At point of origin an irregular, somewhat 
flattened embolus, of a pale colour similar to that of thrombus in 
heart, firmly impacted, not adherent to wall of artery. The 
embolus measures five sixteenths of an inch in its transverse 
diameter, and is three sixteenths of an inch deep. The artery 
beyond and all its branches filled with soft red thrombus, slightly 
adherent to, but easily separable from, the wall. The red colour 
of this contrasts markedly with the pale colour of the embolus, to 
which it is attached above. This is well seen in the specimen 

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(twelve months old) now shown, the natural colours having heen 
preserved by formalin. The corresponding veins, viz. right common 
iliac and its branches, are all completely thrombosed. Left com- 
mon iliac artery and ita branches with the corresponding veins are 

Kidneys. — Both show recent infarcts. The left (6| oz.) shows 
two : (1) a larger one, triangular in shape, base half an inch wide, 
depth half an inch, with an outer deeply congested zone one eighth 
of an inch wide, and a central yellowish and pale zone a quarter 
of an inch wide, extremely well marked, as still well seen in 
specimens shown ; and (2) a smaller one, three sixteenths of an 
inch wide at base and three sixteenths of an inch deep, showing 
similar zones. The right kidney (6 oz.) shows a much larger 
infarct extending along surface from hilus of kidney to extreme 
periphery. In length this is 2\ inches, width half a inch, and 
depth, as seen on cut surface, half an inch. This shows the same 
central pale and the marginal congested zones. 

Spleen 8i oz., enlarged, soft ; shows two recent infarcts of small 
size, and seven sixteenths of an inch by four sixteenths of an inch 
in anterior border, and a larger one in its posterior border (three 
quarters of an inch by half an inch). 

Bemarks, — The condition of embolism described is sufficiently 
rare to deserve special notice. The occurrence of infarcts in the 
spleen in typhoid fever has long been described. It is stated by 
Fagge to be not uncommon. Suppuration and rupture of such 
infarcts is mentioned in text-books as one of the possible causes of 
acute peritonitis in typhoid fever. But that it is a rare complica- 
tion is clear. For it was only observed in two out of sixty-one 
cases by Murchison, in nine out of 250 cases by Hoffmann, and one 
out of ninety-five cases collected by Norman Moore. 

Infarcts in the kidney are apparently even less frequent. 
Murchison only met with them in two cases ; Hoffmann in ten out 
of 250. 

One of Murchisou's cases is described in our * Transactions * 
(vol. xvi, 1865) ; the patient suffered from diarrhcBa all the time ; 
died about the ninth week suddenly. In spleen were found two 
infarcts the size of chestnuts. Heart is described as " healthy." 

Still more rarely infarcts have been found in the liver. Such a 
case is recorded by Murchison in these 'Transactions' (vol. xv, 
1863), reported on and confirmed by Wilks, where an opaque. 

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yellow mass of the size of a pigeon's egg was found in the liver 
resembling an infarct. 

As regards embolism of large arterial trunks, single cases of 
embolism of pulmonary artery have been described by Fagge (vol. 
xxvii) occurring in fourth week ; by Murchison and by Norman 
Moore. Embolism of arteries of limb has been met with clinically 
in a considerable number of cases, usually followed by gangrene of 

A typical case of this kind, observed clinically, resembling 
that I have now described, is the one described by Dr. Sidney 
Phillips (* Clin. Soc. Trans.,' vol. xxiv, 1891), where the left femoral 
artery was suddenly occluded about the thirty-fourth day. He 
ascribed the occlusion to embolism rather than to thrombosis. The 
action of heart was weak and irregular throughout. 

Another case of embolism after typhoid fever necessitating 
amputation has been described by Dr. Drewitt (* Lancet,' 1890). 

In most of these cases the source of the embolus has only been 
surmised. In only one of them, that described by Dr. Norman 
Moore, do I find mention of ante-mortem clots in heart (Case 28) 
accompanying infarcts in lung and spleen. 

The case which pathologically most closely parallels the one I 
have just described is that described by Murchison (vol. xvi, 1865), 
occurring, however, in typhus fever, not in typhoid — viz. embolism 
of iliac, femoral, and other arteries in a case of typhus complicated 
with oedema and gangrene of lower limbs ; death on forty-first day 
of disease, and twenty-four days after the embolism. In that case 
infarcts in spleen and right kidney were found. ** In left ventricle 
several masses of firm decolourised fibrin slightly adherent." 

November I5th, 1898. 

6. Aneurysm of the splenic artery. {Card specimen.) 

AN aneurysm the size of a cherry was found on one of the 
branches of the splenic just after the main trunk had divided 
up close to the hilum of the organ. The artery was, as usual, very 

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tortaons, but was comparative! j very free from atheroma, and the 
walls of the aneurysm to the naked eye were much like those of a 
healthy artery. There was no evidence of embolism. It is 
remarkable that there was a small aneurysm on one of the 
branches of the right middle cerebral artery, the walls of which 
were also apparently healthy. 

The specimen was removed from a woman, aged 37 years, who 
died from the effects of granular kidney. Her heart weighed 
18 oz. 

In the absence of atheroma and embolism, it seems possible that 
this patient had a condition of vessels approachiug that of 
hypoplasia, and that the high vascular tension, due to her kidney 
disease, had led to a dilatation of the vessel walls. This seems 
probable as the vessels which gave way were both badly supported. 
Dr. Lee Dickinson, in the forty-fifth volume of this Society's 
' Transactions,' recorded two cases of aneurysm due to congenital 
delicacy, and not to acquired disease of the aoi*ta. 

Aneurysms of the splenic artery are seldom recorded. In a 
recent search I could only find about twenty published cases. It 
is highly probable that small ones are by no means rare, for two 
were found in the post-mortem room of St. George's Hospital within 
a few months of each other. The spleuic artery is one of the arteries 
in the body most prone to undergo atheromatous changes, and, 
being badly supported, is therefore disposed to further aneurysmal 

Again, emboli frequently pass through it, as shown by the 
occurrence of splenic infarcts, and probably they not infrequently 
lodge where the artery divides up before plunging into the sub- 
stance of the spleen. The reason why aneurysms of the splenic 
artery, and especially those on its branches near the spleen, are 
seldom seen is probably that the spleen is usually removed 
before the splenic artery is examined, and that the condition of 
the artery is comparatively seldom minutely investigated. 

March 7th, 1899. 

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7. Aneurysm of splenic artery. (Card specimen.) 
By W. S. Lazaeus-Bablow, M.D. 

THE specimen shows an aDeur}'sm with calcareous walls, and 
globular in shape, on tbe splenic artery where it passes from 
the tail of the pancreas. The aneurysm is about the size of a 
filbert, and at the autopsy had an appearance which suggested that 
it was a large calculus. On further examination it was found to 
be full of blood-clot. The artery in the neighbourhood and on the 
proximal side of the aneurysm is highly calcareous and filled with 
thrombus. An aneurysm tbe size of a pea, also with calcareous 
walls and filled with thrombus, is situated on tbe proximal side of 
the main aneurysm, and distant from it about one inch. The 
specimen was obtained from the body of a man, aged 61, who died 
from chronic renal fibrosis. The aorta was excessively thick and 
slightly atheromatous, the cerebral arteries were dilated, and their 
walls were thick but not atheromatous. The morbid condition of 
the splenic artery gave rise to no symptoms. Though atheroma of 
the splenic artery has been recorded in tbe Society's * Transactions ' 
twice by Dr. Ogle (vol. iii, p. 337, 1852, and vol. xi, p. 269, case 3, 
1860), and is itself no very uncommon condition, no example of 
aneurysm of the artery is recorded. According to Lebert (cited 
by Quincke in von Ziemssen's * Cyclopaedia '), out of tbirty-nine 
cases of aneurysm of abdominal arteries, excluding tbe abdominal 
aorta, the superior mesenteric and the splenic arteries were afEected 
ten times, the hepatic artery and its branches eight times, the 
eoeliac and the inferior mesenteric arteries three times, the renal 
artery twice ; in three instances the aneurysms were multiple, in 
thirty-six they were solitary. March 7thf 1899. 

8. An apparent thickening of subcutaneous veins. 
By F. Parkes Webee, M.D., F.R.C.P. 

IF the superficial veins, especially tbe internal saphenous veins, 
be examined in a number of rather thin, cachectic men, it is 
found that in at least some of these cases the vessel walls feel as 
if they were thickened. Occasionally the veins can be rolled about 

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under the finger like solid cords, though thinner than they would 
be if they were thrombosed vessels. I have noticed the condition 
chiefly in men slightly under middle age, and it is certainly not 
necessarily accompanied by any obvious corresponding thickening 
of arteries. When, however, it occurs in arterio-sclerotic subjects, 
it is likely to be set down as a " phlebo-sclerosis," and in syphilitic 
subjects it has probably been at times regarded as a chronic specific 
thickening of the vessel walls. I have endeavoured to find out 
what the cause is of this apparent thickening of veins. 

As far as I have been able to investigate the matter, the 
apparent thickening of the vessel walls noted during life seems to 
be due to a contracted condition of the veins (perhaps sometimes 
merely a result of little blood having at the time to. pass through 
them) in cases where the longitudinal bundles of unstriped muscle- 
fibres, which constitute the inner portion of the tunica media,^ 
happen to be particularly well developed. 

In transverse sections of the veins these longitudinal bundles of 

Fig. 11. 

Transverse section ( x 22) of internal saphenous vein from the right 
thigh of a man aged 25. 

^ Some would prefer saying that this longitudinal muscle lies in the outer 
part of the intima. The distribution of the longitudinal muscle in the internal 
saphenous veins appears to me to vary much in different individuals, and even 
in the two limbs of the same individual. Generally, most of it lies within the 
sone of circularly arranged muscle-fibres, whilst a few bundles, if any, lie with- 
out. Occasionally, however, the greater part of the longitudinal muscle is 
arranged in bundles outside the zone of circular muscle, only very little being 
placed between this zone and the endothelium. 

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muscle-fibres are seen projecting into and narrowing the lumen 
as if they were squeezed together by the circular muscle-fibres 
which form the main portion of the tunica media. This is, I 
believe, not merely a jpoat-morlem appearance due to the action of 
hardening reagents, for it is difficult in any other way to explain 
the condition felt during life. 

I am unable to decide that there is any actual hyperplasia of the 
inner portion of the middle coat, like that described by Comil ^ in 
early stages of varicose veins. The upper part of the internal 
saphenous vein may certainly feel like a thin, hard cord, as I bave 
had occasion to note recently, though the lower portion is varicose, 
but without microscopical examination the exact condition of the 
upper part of the vein in such cases cannot be ascertained. 

In order to find out whether a contracted or empty condition of 
veins can give rise to an apparent hyperplasia of the inner portion 
of the middle coat, part of a vein has been hardened in the 
ordinary way, and a similar part has been hardened (as suggested 
by Dr. Payne) with the lumen artificially distended. Mr. Shattock 
kindly obtained the internal saphenous vein from the thigh of a 
man, about 30 years old, who died under an anaesthetic administered 
for some operation on the neck. A part of this vein he artificially 
distended, and sections were cut of the distended part, and like- 
wise of a similar portion hardened without previous distension. 
The undistended portion shows the typical apparent hypertrophy 
of the longitudinal bundles of the inner part of the middle coat, 
whereas the distended portion of the vein shows nothing remark- 
able. It may, therefore, be concluded that emptiness and contrac- 
tion are, in themselves, sufficient to explain the cord-like condition 
of veins felt during life, a condition which doubtless corresponds 
to the ridges of the longitudinally arranged bundles of muscle-fibres 
seen projecting into and filling up the lumen of the vessels in 
transverse sections after death. 

I am forced, therefore, to come to the conclusion that the reasons 
why this condition is clinically especially noticeable in men about 
30 years' of age, in hospital for wasting diseases, are — (1) That 

* V. Comil, in his article on the " Pathological Anatomy of Varicose Veins," 
^Arch. de phjsiol. norm, et path.,' Paris, 1871, tome iv, p. 602, says that when 
the varicose condition is not very great, on catting open the vein longitudinal 
folds may be noticed, cansed by hypertrophy of the most internal portion of the 
middle tunic, as can be shown by sections. 

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the active muscular employment of a working man gives rise before 
the age of thirty to full development of the unstriped muscle in the 
walls of the superficial veins of the limbs ; (2) that the compulsory 
rest in hospital, diminishing the circulation of blood through the 
limbs, causes some of the superficial veins to be comparatively 
empty and contracted ; (3) that the wasting of subcutaneous fat, 
consequent on disease, allows the superficial veins to be more 
easily felt and rolled about under the finger. 

In some of my sections it appears that the fibrous tissue of the 
inner part of the middle tunic is also increased, and, moreover, 
that there is a proliferation of the endothelial cells of the internal 
tunic (superficially resembling a kind of ** endophlebitis pro- 
liferans"). Both conditions may, however, be merely apparent 
changes, due to the contracted state of the vessel walls. A 
moderate degree of this apparent endothelial thickening was ob- 
served in the left internal saphenous vein of a man aged 25, whose 
right internal saphenous vein is figured here as an example of the 
matter under discussion. Janua/ry Zrd, 1899. 

9. Tuberculosis of the inferior vena cava. {Card specimen). 
By J. H. Deysdale, M.D. 

THE specimen was taken from a man who died of pulmonary 
tuberculosis in St. Bartholomew's Hospital. At the post- 
mortem examination the right supra-renal (capsule was much 
enlarged by fibro-caseous tuberculous deposit. On opening the 
inferior vena cava, where it had been in contact with the enlarged 
adrenal, a number of small tubercles could be seen projecting on 
the inner surface. Tubercle bacilli were demonstrated in micro- 
scopical preparations. May l^th, 1899. 

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1. Actinomycosis of the tongue. 

Exhibited by E. G. Hebb, M.D., for Mr. Ludfoed Cooper. 

THE patient, T. D — , aged 60, a naval pensioner, was admitted 
to St. Bartholomew's Hospital, Rochester, under the care of 
Mr. Ludford Cooper, having been sent up for opinion by Fleet- 
Surgeon Sweetman. He stated that he had noticed a " small lump 
under the tongue for some time, but cannot say how long." Some 
months ago there was *^ a little crack in the middle of the tongue." 
He has often been in the habit of picking " bits of things,*' 
flowers, straws, <&c., and putting them in his mouth. He has been 
a great smoker. There is no history of venereal disease. He has 
not wasted, and has had no pain in his tongue. His mother died 
of "cancer of the breast," and his father, at seventy-seven, of 
" old age." The patient is a healthy looking man, and, bar the 
tongue, nothing abnormal was discovered after careful examination. 
On the dorsum of the tongue, exactly in the middle line, and 
about one inch from the tip, is a swelling about the size and shape 
of an almond, with slightly indurated edges. There is apparently 
no fluctuation in the tumour. There are no enlarged lymphatic 
glands. As it was a doubtful looking tumour, and although 
possibly a gumma, it was thought proper, taking into consideration 
the patient's ago, to excise the tongue. Accordingly Mr. Cooper 
removed the tongue by Whitehead's method on August 25th, 1898. 
The patient was discharged quite well on the eleventh day after 
the operation. Micro-sections show the tumour to be a spheroidal 
mass with a diameter of about half an inch. It is composed of 
small round cells, in which lie embedded a few irregular-shaped 
masses of the ray fungus, with characteristic club-shaped elements. 
In the sections, which are stained with logwood and rubin, the 

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tuinour is represented by its peripheral zone, the central portion 
being absent. 

The microtomist informed me (R. G. H.) that when he incised 
the tumour the central portion was found to contain a yellow 
purulent fluid, which was thrown away without examination. 

October 19th, 1898. 

2. Cohffenital cyst of the base of the tongue. 
By Raymond Johnson. 

THE specimen exhibited consists of the tongue and adjacent parts 
removed from a male child aged four months. Since birth 
some difficulty of breathing had been noticed ; this had gradually 
increased until severe choking fits occurred during sleep, and 
difficulty in swallowing was also present. When admitted to the 
Victoria Hospital for Children the child was pale and emaciated ; 
there was stridor and marked recession of the lower ribs during 
inspiration. With a finger in the mouth a smooth, elastic swelling 
as large as a cherry could be felt at the back of the tongue imme- 
diately in front of the epiglottis. Tracheotomy was performed, 
but the child died a week later. 

The specimen has been divided by a sagittal section. Occupying 

Fig. 12. 

the extreme posterior part of the tongue, and placed exactly in the 
middle line, is a cyst, which projects on the surface as a smooth 

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bemispherical swelliDg about 1*5 cm. in diameter. The postero- 
inferior surface of the cyst lies in contact with the anterior surface 
of the epiglottis, the latter being so much pushed backwards as 
nearly to occlude the upper aperture of the larynx. The anterior 
border of the cyst lies immediately behind the circumvallate 
papillae, and no indication of the position of the foramen caecum 

Fig. 13. 

The outline of the cyst in section is almost semicircular, the 
antero-inferior or deep aspect of the cyst being flattened. The 
lowest part of the cyst is 3 mm. distant from the hyoid bone. The 
inner surface is smooth, but in the centre of the antero-inferior 
flattened aspect of the cyst wall there is a small depression, which 
is the orifice of a short canal in the substance of the tongue. In 
the left half of the cyst some of the coagulated contents, probably 
mucoid in character, still remain. 

Examined microscopically, the cyst is found to be lined with a. 
thin layer of stratified epithelium, between which and the muscular 
tissue of the tongue, in which the cyst is embedded, is a layer of 
fibrous tissue forming a definite cyst wall. In the muscular sub- 
stance around the cyst are the large and deeply placed mucous 
glands which are naturally present in the part. 

Cysts in the base of the tongue may arise in the large mucous 
glands which open on its surface, or in connection with the upper 
part of the lingual duct or its glandular appendages. Cysts 
belonging to the latter gi'oup have been carefully investigated by 
Dr. Martin B. Schmidt, of Strasburg (* Ueber die Flimmercysten 
der Zungenwurzel und die drusigen Anchange des Ductus Thyreo- 
glossus,' 1896). He describes the glandular appendages of the 
lingual duct as occurring in two forms : (1) Deeply placed mucous 
glands which open into the duct, and (2) branching tubular spaces 

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comtnunicating with the duct. These tubes and the ducts of the 
mucous glands contain ciliated epithelium. 

From these structures cysts may arise. They are usually 
multiple, contain mucus, and are lined with an epithelium which 
in part at least is ciliated. In the majority of the specimens of 
such cysts examined by Schmidt there was no external evidence of 
their presence, and the cysts were only discovered on making 
sections of the organ. 

The occurrence of tumours — sometimes cystic — at the base of 
the tongue having the structure of the thyroid gland is now 
thoroughly established. They must be regarded as accessory 
thyroids developing in connection with the upper end of the 
thyreoglossal duct, just as such accessory thyroids are known to 
develop around its infra-hyoid segment. 

An extraordinary case, showing that such a lingual thyroid may 
be functionally active, has been recorded by Seldowitsch (* Central- 
blatt ftir Chirurgie,' 1897, p. 499). The patient was a girl of 14, 
and the removal of the tumour was followed by the characteristic 
symptoms of myxoedema, which disappeared under the administra- 
tion of thyroid extract. No thyroid gland could be felt in the 
neck, and it was assumed that the ** tumour *' of the tongue repre- 
sented the only thyroid tissue which the patient possessed. 

My own specimen is undoubtedly a mucous cyst, but from the 
microscopic examination it does not seem possible to decide upon 
its exact origin, and it is conceivable that it arose from some of 
the superficial or deep sets of mucous glands. Three points may, 
however, be .noted: (1) That the cyst is seated exactly in the 
middle line of the tongue, immediately behind the circumvallate 
papillae ; (2) that no foramen caecum is recognisable ; and (3) that 
the cyst is single, and presents no evidence of having arisen by the 
confluence of smaller cysts. For these reasons I would suggest 
that the cyst has arisen by distension of the extreme upper part of 
the lingual duct. April Uh, 1899. 

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S.u\/)1 I 


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Illustrating Dr. Hugh Walshaon's paper on Epithelial Pearls in 
the TonsU. (Page 65.) 

Fia. 1. — Section through tonsil of a male aged 27. Three pearls are seen 
embedded in the adenoid substance of the tonsil. The middle pearl b partially 

Fia. 2. — Section through tonsil of a male aged 31. It shows an epithelial 
pearl in the adenoid tissne of the tonsil. There is no evidence of calcification. 

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3. Epithelial pearls in the tonsil. 

By Hugh Walsham, M.A , M.D. 

[With Plate III.] 

THE late Professor Eantback,^ in a very interesting paper in the 
* Illustrated Medical News ' of November 9th, 1889, and also 
in a paper in the * Journal of Anatomy and Physiology/ calls 
attention to the occurrence of epithelial pearls in the tonsils of 
human foetuses and new-bom infants, and points out that they 
occur as retentions and not as embryonic inclusions, thus differing 
altogether from the epithelial pearls described by Mr. Bland 
Sutton (in his lectures on "Evolution in Pathology "), which are 
found in the middle line of the palate and in other parts. 

Professor Kanthack says that he has found these retention pearls 
also in the tonsils of young persons, the oldest being 17 years of 
age. Their occurrence in adults is not altogether rare, and while 
making some observations on the occurrence of tubercle in the 
tonsil I met with three very good specimens in the tonsils of men 
aged 27, 31, and 35 years respectively. The occurrence of these 
pearls in the organ is of interest, because I think there can be no 
doubt that they are the origin of at least some of the so-called 
tonsil calculi. The accompanying drawings show very clearly these 
interesting bodies. 

Fig. 1 is a microscopical section through the tonsil of a male 
aged 27. Three of these pearls are seen, the middle one showing 
evidence of calcification. The centre of the pearls shows no 
definite structure ; it is only on carefully examining the periphery 
that we see that they are composed of horny, squamous, epithelial 
cells pressed tightly together. They bear a close resemblance to 
the epithelial cell nests found in some of the squamous-celled car- 

Fig. 2, from a male aged 31. The section shows another of these 
ctirious bodies, which is probably not so old as the former 
specimens, as the cells can be traced nearly to the middle of the 

* Kanthack, * Journ. of Anat. and Phjiiol.,* vol. xxvi. 


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pearl. The occurrence of these bodies, as before said, is not alto- 
gether rare, but the above are the only examples met with in 160 
post-mortem examinations of the tonsils with reference to their 

But in addition to these epithelial pearls we find what are 
apparently true epithelial inclusions, which, as far as I know, have 
not yet been described in this country. They consist of isolated 
epithelial accumulations in the adenoid tissue of the tonsil. Great 
care is required in looking for these bodies, lest we mistake for 
them some portion of the epithelial lining of one of the crypts 
which has been cut obliquely. After uterine life we must also 
remember that the lymphocytes pass right amongst the epithelium, 
and may thus lead to fallacies. I am quite satisfied, however, that 
such isolated islets of epithelium do exist, resembling those 
epithelial accumulations which are found in the middle line of the 
palate, penis, and in other places. 

Professor Retterer ^ has also observed these epithelial accumula- 
tions in the adenoid tissue of the tonsil, and believes they are 
formed by epithelial detachments from the base of the primary 
invagination during the development of the organ. In St-ptem- 
ber, 1898, 1 sent a short paper to the * Lancet,' published in April, 
1899, on the occurrence of epithelial pearls in the tonsil. I said 
there, in reference to these epithelial accumulations, that they could 
not be regarded either as retention or inclusion products. I have 
been working at the subject since then, and I think the explanation 
given above to be the true one — that is, that they are true embryonic 
inclusions. November 1st, 1898. 

4. A tumour arising in the region of the socia parotidis, 
{Card specimen.) 


A WOMAN, aged 56 years, had noticed a tumour in the right 
cheek for fifteen years. It grew steadily until a year before 
removal ; it then increased rapidly and doubled its size. It reached 

* Retterer, " Origine et Evolution de» amygdMles chez les mammifferes," 
* Journ. de I'anat. et de la phys./ 1888, vol. xxiv, p. 1. 

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the size of a small orange and projected into the mouth. On 
examination it had an elastic, semi-solid feel. 

After removal it was found to be an encapsuled cystic tumonr. 
The fluid from the cysts contained cholesterin, but did not give the 
chemical tests for mucin. 

Histologically the tumour is a cystic myxo-fibro-adenoma. The 
cystic spaces are of considerable size and are lined by cubical 
epithelium, and closely resemble the cysts in common cystic fibro- 
adenoma of the breast. In parts the cysts contain homogeneous 
material. There is a fair amount of interstitial tissue ; some of 
this is ordinary myxomatous tissue. There are also areas of closely 
packed cells, probably immature epithelial cells. In places the 
fibrous tissue is of an adult type and has undergone hyaline 
change. Occasionally these strands of hyaline degenerated fibrous 
tissue show a concentric arrangement. The structure of the 
tumour resembles that often seen in parotid tumours, but is more 
markedly cystic. May 2nd, 1899. 

5. AdenO'lipoma of the submaxillary salivary gland. 
By H. J. Wabino, M.S. 

NON-MALiGNAJfT tumours of the submaxillary salivary glands 
are uncommon, and when met with they generally have the 
structure of mixed tissue tumours such as those which are frequent 
in the parotid salivary gland. The tumour, a section of which is 
shown in Fig. 14, has a different structure, and was removed 
from the submaxillary region of a young man aged 22; it had 
been present for at least five years, and had grown steadily but 
slowly. A short time before it was removed the rate of growth 
had somewhat increased. The tumour, which was removed 
through an incision in the submaxillary region, was situated 
underneath the deep fascia in the submaxillary triangle, and was 
apparently attached to the superficial lobe of the submaxillary 
salivary gland, where it lies on the surface of the mylo-hyoid 
muscle. In shape the tumour was elliptical or egg-shaped, and 
in size its long axis measured two and a half inches, and its short 

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one, one and a quarter inches. The tumour had a distinct capsule 
of fibrous tissue, and was easily and readily separated from the 
submaxillary salivary gland and the surrounding tissues. 

Fro. 14. 

a. Glandular acini, b. Section of a dact. c. Fat cells, d. Connective tissue 
and blood-vessels. 

The structure of the tumour is well shown in the figure. It 
consists of a basis of fatty and connective tissues, and amongst 
these are numerous islands of glandular tissue, which resemble to 
a certain extent histologically the structure of a normal salivary 
gland. The glandular acini are very distinct, and in places sections 
of what appear to be ducts are visible. Around some of the ducts 
there is a considerable accumulation of connective-tissue cells and 
fibres. May 2nd, 1899. 

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6. Idiopathic hypertrophy of the (Esophagus. 


THIS condition was found accidentally in the course of an 
autopsy on a patient of Dr. Ewart's, to whose kindness I am 
indebted for leave to bring the specimen forward. The patient's 
daughter, who had had her meals with him, was carefully 
questioned, and could not remember that he had ever complained 
of any pain or difficulty in swallowing, or that he had ever suffered 
from regurgitation of food after eating. 

He was a man 59 years of age, who died with erysipelas and 
bronchitis after fractured ribs. The kidneys were red and 
granular. The heart, 14 ounces, showed hypertrophy of the left 
ventricle. There was also some hypertrophy of the prostate. The 
oesophagus was not increased in length or dilated in any part of 
its course; its lumen was not narrowed, and there was not the 
slighteRt trace of a stricture in any part of the tube. Three inches 
below the cricoid cartilage the circular muscular coat began to be 
hypertrophied ; this hypertrophy regularly increased along the 
course of the oesophagus towards the stomach, but there was no 
excessive increase in this hyperplasia of the muscular coat near the 
cardiac orifice, such as might have been expected if there had been 
chronic spasm of the cardiac orifice. The oesophagus was affected 
right up to its entrance into the stomach. This is a point of 
importance as bearing on the possibility of the hypertrophy being 
due to spasm of the diaphragm. If there had been spasm of the 
diaphragm leading to oesophageal obstruction, the portion of the 
oesophagus below the diaphragm would not necessarily share in the 
hypertrophy above. 

The hypertrophy was practically limited to the circular muscular 
coat, and microscopically no evidence of fibrosis or inflammation 
was found. The mucosa of the oesophagus was opaque, but was 
not specially affected with chronic oesophagitis. It separated 
readily from the underlying coats, and no sign of ulceration or 
growth could be found in it. There were a number of adhesions 
around outside of the affected part of the oesophagus, but they were 

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not dense or sufl&cient to embarrass the contraction of the 
oesophagus, and did not seem in any way to account for the hyper- 
trophy of the middle coat. There was no stricture of the cardiac 
orifice ; the stomach was rather larger than natural, but presented 
no gross Jesion. The pyloric orifice was certainly small, but there 
was no morbid thickening of its walls. No morbid change in the 
diaphragm was noticed. 

Bemarks. — ^This remarkable condition of idiopathic hypertrophy 
without accompanying dilatation, to which I have failed to find any 
reference, appears to have given rise to no symptoms during life ; 
it is, therefore, hardly necessary to raise the question whether it 
was associated with any clinical condition such as rumination of 
food or cardiospasm. In both these affections dilatation of the 
lower end of the oesophagus probably results, but it does not appear 
that hypertrophy occurs, though it would be natural to expect some 
hypertrophy as compensatory to and as a result of dilatation. 
That there must have been a cause, and that the hypertrophy is 
only apparently idiopathic, is of course true. Cardiospasm naturally 
at once suggests itself as a cause of this hypertrophy, but there is 
absolutely no proof that such a condition existed during life in this 
case, or even, probable as it would appear from a priori, that 
hypertrophy of the lower end of the oesophagus occurs in cardio- 
spasm. In vol. xlvii of the Society's * Transactions '^ I described 
a case of marked dilatation of the oesophagus in a boy aged 8 years, 
who came of a neurotic stock. There was no organic cause, such 
as stricture, to account for the dilatation and hypertrophy, and I 
then suggested that possibly a failure in the co-ordinating 
mechanism, by which the cardiac sphincter is relaxed during 
swallowing, might by producing obstruction be the cause of the 
changes in the oesophagus. The non-relaxation of the cardiac 
sphincter might be due to paralysis or to inhibition of the longi- 
tudinal fibres of the oesophagus ; in either case the circular muscular 
fibres would have more work to do on driving the food into the 
stomach, and upon this view the hypertrophy could be explained. 
It appears to me that this explanation of non-relaxation of the 
cardiac sphincter is one that may also be applied in the present case. 
At any rate, whatever the resistance to the passage of food was, the 
hypertrophy of the circular coat of the oesophagus fully com- 
pensated for it, and so no difficulty was experienced during life. 

» Page 37. 

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The man was cut off by intercurrent disease before this com- 
pensatory hypertrophy failed and gave way to dilatation. This 
specimen is, therefore, an early stage of the condition of combined 
dilatation, and hypertrophy of the oesophagus, of whkh a certain 
number are to be found in literature and in museums. 

The subjects of this disease may live for a long time with 
symptoms, such as vomiting, pointing definitely to the gastro- 
intestinal tract, though even this is a rare condition. I am not 
aware that any specimen of "idiopathic" hypertrophy without 
dilatation has been described. November Ist, 1898. 

7. Fusiform dilatation of the oesophagm. 
By W. S. Lazabus- Barlow, M.D. 

THE specimen under consideration was obtained from the body of 
a man, aged 28 years, who died in St. George's Hospital. 
He was admitted nine days before death for extreme emaciatioui 
together with epigastric pain and tenderness. The history was 
very indefinite, but the patient said that twelve months previously 
he had had ** difficulty of swallowing and tubes were passed" down 
his oesophagus. He also stated that at that time he suffered from 
frequent vomiting. On admission it was found that his epigastric 
pain bore no distinct relation to ingestion of food, that he suffered 
severely from dysphagia, that ingested food was returned imme- 
diately and unchanged. The vomit was acid, and contained mucus 
besides the unaltered food. Bougies were passed, but no obstruc- 
tion was encountered, though they entered as far as 17 inches. 
On the fifth day after admission laparotomy was performed, on the 
suspicion that there might be disease of the stomach, but nothing 
abnormal was found in the stomach or elsewhere. Three days 
later the patient died of asthenia. 

At the autopsy it was found that there was a generalised miliary 
tuberculosis. The total amount of tubercular disease in the body 
was not great, and the chief seat was in the lungs, and especially in 
the left upper lobe. Bi?sides implication by tubercle, the left lung 

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was the seat of a patchv pneumonia in the stage of red hepatisa- 
tion, and the right lung was engorged and cedematous. 

Over its middle five sevenths the oesophagus was dilated in fusi- 
form fashion, and contained much slightly modified food. At the 
widest part the circumference was three and a half inches, corre- 
sponding to a circular tube with a diameter of one inch. The 
mucous membrane was shreddy, and the muscle of the tube was 
greatly hypertrophied. At the cardiac end the oesophagus was 
narrower than elsewhere, but there was nothing approaching to 
stenosis. Microscopically the muscle of the oesophagus had under- 
gone no change that was not in all probability due to post-mortem 
decomposition, with exception of the hyperplasia of muscular 
elements. The cell protoplasm, it is true, was highly granular and 
the actual muscle bundles broken up in many places, but the nuclei 
everywhere stained well. There was no abnormal predominance 
of circular fibres or inferiority in numbers of longitudinal bundles. 
The shreddy condition of the oesophageal mucous membrane and 
the general absence of epithelium were in favour of the view that 
the muscular changes were of post-mortem origin. Nevertheless 
it must be mentioned that the autopsy was made only ten hours 
after death, and that death took place during the month of 

Remarks. — The dilatation, though sufl&ciently marked, is by no 
means so great as has previously been recorded. Dilatations with 
circumferences of 5 J inches, 6 inches, and 6| inches have 
been recorded by Barker,^ Wardrop GriflSth,*-^ and Wilks 
and Roote* respectively, but the cause of the dilatation, as in 
other recorded cases, is quite uncertain. Rolleston* has suggested 
that possibly that stenosis on the distal side of the dilatation and 
hypertrophy which is apparently demanded by the fundamental 
laws of pathology governing dilatation and hypertrophy, may be 
relative rather than actual, and may depend upon a faulty contrac- 
tion of the longitudinal muscle bundles at the lower end of the 
oesophagus by which its dilatation is normally brought about. 
Langley^ has also recently shown that stimulation of the vagus 

» Barker, 'Trans. Path. Soc./ vol. x, 1859, p. 141. 

« Wardrop Griffith, * Med. Chron..' Nov., 1898. 

' Wilks and Roote, • Trans. Path. Soc.,* vol. xvii, 1866, p. 138. 

•• Rolleston. « AUbutt's Syst. of Med.,' art. " Diseases of the (Esophagus." 

5 Langley, * Journ. of Pbysiol./ vol. xxiii, 1899. 

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leads to dilatation of the lower end of the oesophagus in the cat. 
It therefore seemed advisable in the present case to investigate the 
condition of the vagus, and Br. O. P. Qrunbaum made sections of 
the nerve in various parts of its course in order to determine if 
possible whether there were present signs of recent or of old 
degeneration. So far as can be seen, there is no definite evidence 
that the nerve was abnormal ; nevertheless it is difficult to describe 
it as normal, though the greatest care was taken in its preparation, 
because the fibrous tissue which would fill up the former seats of 
nerve fibrils if there were degeneration of old standing, would be 
impossible to distinguish from the connective tissue already present 
between the individual bundles of nerve fibrils. 

The specimen is preserved in the museum of St. George's 
Hospital, No. 5081. February 7th, 1899. 

8. Myoma of the oesophagus. {Card specimen.) 
By H. B. RoLLESTON, M.A., M.B. 

A SMALL white tumour growing in the submucosa and rather 
more adherent to the muscular than to the mucous coat. It 
was about the size of a cherry, and microscopically was a pure 
leiomyoma. It was probably derived from the circular muscular 
coat. It was situated at the junction of the upper and middle 
thirds of the oesophagus in a woman, aged 49, who died of influenzal 
broncho-pneumonia. It had not giren nse to any clinical symptoms. 
There were no uterine myomata. March 7th, 1899. 

9. Minute erosion {exulceratio simplex) of the gastric mucous 
membrane. {Card specimen.) 

By H. B. RoLLBSTON, M.A., M.B. 

AN ansBmic woman, 25 years of age, who had suffered from 
Tomiting after meals for thrde weeks, was admitted under my 
care at St. George's Hospital two days after bringing up 3 ounces 

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of blood. On examination the abdominal muscles were flaccid and 
a pulsating aorta was felt, but there was no tenderness on exerting 
pressure over the stomach. I was inclined to regard the case as 
one of gastritis rather than gastric ulcer, and the patient was 
therefore allowed milk and beef tea bv the mouth. Two days after 
admission she brought up as much as two and a half pints of blood. 
After this she was fed entirely per rectum^ and went on well until 
eight days later, when she quite suddenly died. 

At the pott-mortem death was found to have been caused by 
pulmonary embolism, the source of the embolus being thrombosis 
in the left external iliac vein which had not attracted any attention 
during life. The stomach shows two small elongated abrasions of 
the mucous membrane measuring not more than a quarter of an 
inch in length by one eighth of an inch in breadth. Both these 
erosions are close to the lesser curvature, one on the anterior, the 
other on the posterior surface of the stomach, about 2 inches from 
the oesophageal opening. These abrasions are therefore opposite 
to each other. That on the posterior surface has opened into a 
vessel, and from it no doubt the hsemorrhage came. The other 
abrasion on the anterior surface is for the most part cicatrised. 
There was no varicosity of the gastric veins. 

This superficial erosion of the gastric mucous membrane has 
recently been specially described by Dieulafoy,i who gave the 
name exulceratio simplex to this condition, which he regards as an 
early stage of the ordinary gastric ulcer, and by Lindsay Steven,^ 
who had two fatal cases of profuse heematemesis from this lesion 
which he terms ** pore-like " erosion of the gastric arteries. 
Dieulafoy had seven cases, and Lindsay Steven ^ refers to previous 
cases belonging to this category recorded by Murchison (in 
vol. xxi of this Society's 'Transactions'), Chiari, and Perrand. 
Deguy ^ has recently described a small superficial abrasion eight 
tenths of a millimetre in a man who died of hsematemesis, and who 
had latent hepatic cirrhosis. From these cases it appears that the 
haemorrhage is extremely profuse, and that it has been directly 
fatal, while other signs of gastric ulceration may be absent. 

If, as seems not unlikely, this lesion is the first stage of an 
ordinary gastric ulcer, it must be common, but it may be so small 

1 Dieulafoy, ' La Presso M^dicale/ Jan. 19th, 1898. 

' Lindsay Steven, 'Glasgow Mt^d. Journ.,' vol. li, p. 5, Jan., 1899. 

» Deguy, • Bull. Soc. Anat.,' Paris, Dec, 1898. 

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as to be overlooked, wben it proves fatal, and often, of course, goes 
on to the further stage of a deep ulcer. March 2l8t, 1899. 

10. Gastric ulcer from a patient with granular kidneys. 
{Card specimen.) 


THE whole stomach was very greatly engorged. Surrounding the 
pylorus there was a recent ulcer 2 inches by 1 inch. Micro- 
scopically the vessels on the floor of the ulcer were much dilated 
and full of blood ; in places there were small haemorrhages into 
the submucous coat. There was do pigmentation, however. There 
were some haemorrhages into the mucous membrane of the ileum, 
but no ulcers there. Prom a woman aged 37 years, who had 
granular kidneys, and small aneurysms on the splenic (vide p. 56) 
and right middle cerebral arteries. 

Remarks. — The ulcer was recent, and it appears probable that it 
may have been brought about as the result of haemorrhage taking 
place into the mucous and submucous coats of the stomach, the 
haemorrhage being analogous to retinal haemorrhages. This form 
of ulceration was described by Dr. W. H. Dickinson, who in his 
paper in the * Transactions * of the Eoyal Medical and Chirurgical 
Society (vol. Ixxvii, p. Ill, 1894) found, in the course of forty 
years' experience of post-mortem examinations at St. George's 
Hospital, twenty-two cases of ulceration of the intestines and three 
examples of gastric ulcer in chronic nephritis. There is no reason 
why renal disease should protect the patient from ordinary gastric 
ulcer, but I am rather inclined to regard the recent ulcer in this 
case, associated as it was with haemorrhage into the submucous 
coat, as definitely related to the renal disease, and not as a mere 
coincidence. March 7th, 1899. 

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11. Tubercular ulcer of the stomach in children. 
By Qeobgb R Still, M.D. 

TUBEBCULAB ulcer of the stomach is an occurrence of considerable 
rarity, and very few cases have been recorded by English 
writers. I venture, therefore, to show specimens of this condition 
taken from five cases which I have met with at the Hospital for 
Sick Children, Great Ormond Street. 

In three of these cases a microscopic examination was made, and 
the typical appearances of tubercular ulceration with characteristic 
giant-cells were found, and in two cases tubercle bacilli were 
demonstrated in the base of the ulcer. lu the remaining two cases 
no microscopic examination was made, as it was desired to preserve 
the specimens for the n^useum, but the naked-eye appearances 
were such as to leave, I think, no doubt whatever that these also 
were tubercular ulcers. 

Case 1. — George P — , aged Si years at death. Seven months 
previously ascites and oedema of the legs appeared, and there was 
some vomiting. Paracentesis abdominis was done three times, 
but the abdomen remained very full and resisteut, and although 
fluid did not reaccumulate after the third tapping, the abdomen 
had the doughy feeling of tubercular peritonitis on palpation. 
There was occasional vomiting throughout the illness, sometimes 
on several consecutive days, but sometimes only after an interval 
of two or three weeks. Pulmonary symptoms developed, the child 
gradually emaciated, and after seven months' illness died. With 
the exception of the vomiting, which may have been due to the 
tubercular peritonitis, there were no symptoms pointing specially 
to gastric ulcer. 

Post-mortem, — There was extensive tubercular peritonitis with 
adhesions. There was some tubercular ulceration of the lower 
part of the ileum and just below the ileo-caecal valve, but no 
ulceration higher up in the small intestine. The stomach was 
adherent to the liver and to the surrounding structures ; it was not 
noticeably dilated. On the posterior wall of the stomach just 
below the lesser curvature, about 4 cm. to the left of the pylorus. 

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was a small ulcer somewhat irregular in shape, and about 2 mm. in 
width at its widest part. Its edges were hardly definitely 
thickened, and the ulcer was so small that it was difficult to judge 
of the character of its base, but it was evident that the ulceration 
extended deeply, though not actually exposing the muscular layer. 
Some lymphatic glands along the lesser curvature of the stomach 
were enlarged and ca«eous. There was extensive tuberculosis of 
the lungs and of the mediastinal and mesenteric glands. 

Microscopic examination showed an area of small round-cell 
infiltration, with several giant -cells in the submucosa, forming the 
base of the ulcer over which the mucous membrane had dis- 
appeared. The area of inflammation undermined the mucosa for 
a shoi-t distance at the edge of the ulcer, and here there was some 
round-cell infiltration of the mucosa itself. Tbe muscular coat was 
normal. In the subperitoneal tissue outside the muscular layer 
several small foci of tubercular deposit were seen. Two or three 
tubercle bacilli were found in the base of the ulcer after carefully 
searching through several sections. 

Case 2. — ^John L — , aged 10 months at death. After four weeks* 
illness with cough he showed signs of consolidation in the lungs, 
and then symptoms of tubercular meningitis supervened, and he 
died five and a half weeks after the onset of the illness. Vomiting 
was frequent during the last ten days of life, but there was nothing 
otherwise which might have suggested gastric ulcer, and the 
vomiting may have been entirely due to the meningitis. 

Post-mortem. — There was general miliary tuberculosis affecting 
the meninges, lungs, and almost every organ in the body. There 
was no definite peritonitis, and no peritoneal adhesions. Only four 
tubercular ulcers were found in the ileum. The stomach showed 
on the lesser curvature about 1'5 cm. from the pylorus a small 
ulcer, roughly circular in shape, about 3 mm. in diameter, with the 
edges thickened and vascular. No tubercle could be seen on the 
peritoneal surface. 

Microscopic examination showed a small area of round-cell 
infiltration forming the base of the ulcer in the submucosa, and 
slightly invading tbe mucosa at the edge of the ulcer. The vessels 
of tbe submucous layer in the neighbourhood of tbe ulcer were 
dilated. The muscular coat was normal, and no tubercular deposit 
was seen in the subperitoneal tissue. 

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No giant-cells were fouud in the base of the ulcer, but very 
numerous tubercle bacilli were present here, their large number 
contrasting markedly with the scarcity of bacilli in Case 1 and in 
the following case. 

Case 3. — Elsie W — , aged 3 J years. The abdomen had been 
enlarged for two years, and there had been occasional vomiting. 
On admission the abdomen was full and resistent, and there were 
signs of consolidation in both lungs. The child gradually became 
emaciated, symptoms of tubercular meningitis supervened, and 
death occurred nearly four weeks after admission to the hospital. 
While the child was under our observation there was only occa- 
sional vomiting, and nothing otherwise to suggest gastric ulcer. 

Fost-mortem, — In addition to some tubercular meningitis and a 
caseous mass in the right optic thalamus, and some not very 
advanced tuberculosis of the lungs, there was much tubercular 
peritonitis with adhesions completely obliterating the peritoneal 
cavity. Examination of the intestine was difficult owing to the 
matting, but the greater part of the small intestine and almost all 
the large intestine was examined, and only one slight erosion was 
found in the ileum, none elsewhere. The stomach was adherent to 
the liver and to the surrounding structures. It was normal in 
49ize. A small ulcer, about 2 to 3 mm. in diameter and circular in 
shape, was found about 1*5 cm. below the cardiac orifice on the 
posterior wall of the stomach. Its edges were thickened ; it seemed 
to pass through the submucosa, but not through the muscular 
wall. On the outer surface, which was here closely adherent to 
the diaphragm, there was a small caseous plaque. Another much 
more superficial erosion, with some vascularity of the surrounding 
mucous membrane, was present about 3*6 cm. nearer to the pylorus 
on the lesser curvature. Microscopic examination showed an area 
of round-cell infiltration in the submucosa forming the base of the 
ulcer, and extending partially through the muscular layer. At the 
margin of the ulcer there was also some slight infiltration of the 
deeper part of the mucosa. Giant-cells were present in the base of 
the ulcer, but careful search revealed only one very doubtful 
tubercle bacillus. 

Case 4. — Daniel P — , aged 2 years and 8 mouths. There had 
been vomiting, with gradual emaciation, and enlargement of the 

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abdomen for two months. There had also been some tenderness 
of the abdomen, which on admission was full and unduly resistent. 
With the exception of the vomiting, and possibly the tenderness 
of the abdomen, there were no symptoms specially pointing to 
ulceration of the stomach. The child died three days after admis- 
sion to the hospital, and during that time there was no vomiting. 

Post-mortem. — ^There was extensive tuberculosis of the lungs and 
other organs, not of the acute miliary type, but rather chronic, 
with a tendency to caseation. Early tubercular peritonitis was 
present, with some adhesions, and probably also some superadded 
acute septic peritonitis due to perforation of a tubercular ulcer in the 
ileum, which had allowed fseces to escape into the peritoneal cavity. 
The small intestine was extensively ulcerated as high up as the 
lower part of the duodenum. 

The stomach was not noticeably dilated. Close to the lesser 
curvature and situated halfway between the cardiac orifice and the 
pylorus on the posterior wall was a tubercular ulcer with its long 
axis parallel to the upper border of the stomach, and measuring 
1-6 cm. transversely and nearly 1 cm. from above downwards. Its 
edges were thickened, but less than usually happens in a tubercu- 
lar ulcer of the intestine (a feature of the gastric tubercular ulcer 
to which the late Professor Coats ^ drew attention), and its base 
was of a yellowish grey coloui-, and rough. On the peritoneum 
outside the ulcer a grey tubercle was seen. No microscopic exami- 
nation was made as the specimen was preserved for the museum. 

Case 5. — James T — , aged 9 years. Two years ago he suffered 
with vomiting and diarrhoea ; subsequently a serous pleural effusion 
occurred on one side of the chest, and later still the abdomen 
became full and resistent ; there was gradual emaciation, and some 
vomiting two mouths before death, but none later, and no other 
symptoms pointing to gastric ulcer. 

Post-mortem. — There was extensive tuberculosis of almost all the 
organs. The peiitoueal cavity was completely obliterated by adhe- 
sions, with much caseous material in the adhesions. Both the small 
and large intestines were much ulcerated. The stomach showed on 
the lessor curvature, near the cardiac opening, a small cicatrix, the 
external sui-face here being closely adherent to the liver. It seemed 
probable that it was the scar of a tubercular ulcer. Just below 
^ * Gliisgow Me»l. Joorn.,* 1886. p. 54. 

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the lesser curvature, near the pylorus on the posterior wall was a 
small ulcer about -5 cm. in diameter, round, with slightly thickened 
edge, and roughened base, which did not expose the muscular 
layer. Between this and the cardiac opening was another depres- 
sion on the anterior wall of the stomach, and at the bottom of this 
depression was a small pierf oration through which a probe passed 
into dense adhesions outside the stomach. The specimen was 
preserved for the museum, so no microscopic examination was 

These five cases of tubercular ulcer of the stomach are the only 
cases I have met with in 206 autopsies on children with abdominal 
tuberculosis, or in 226 tubercular cases if those be included in 
which the abdomen was not affected. 

The statistics of other writers show a similar rarity ; including 
all varieties of tuberculosis in children, Widerhofer (1) found 
tubercular gastric ulcer twice in 418 cases, Steiner and Neureutter 
(2) four times in 302 autopsies, Eilliet and Barthez (3) 21 times in 
141, and more recently Holt (4) found gastric ulcer 6 times in 119 
cases, but states that the evidence was not conclusive in all of them 
that the ulcers were tubercular. 

Unfortunately in several of the published cases and statistics no 
satisfactory evidence of the tubercular nature of the ulcer has 
been given, so that some doubt attaches to them. Occasionally in 
children with tuberculosis ulceration of the stomach is present, 
which on microscopic and bacteriological examination shows no 
evidence of a tubercular nature, any case therefore which has not 
been verified thus must be received with caution. Two of my 
cases are open to this objection, but, as I have already stated, the 
naked-eye appearances were such as to leave little doubt that they 
were really tubercular. 

Only two cases of tubercular ulcer of the stomach have been re- 
corded in the Transactions of this Society (5), both in adults. A 
case of ulceration of the stomach in a female infant aged twenty- 
one months, who died with tuberculosis, was described by Dr. 
Barlow (6), but he considered it by no means certain that the 
tilcers were really tubercular, and stated that he had seen three 
other similar cases in children where the nature of the ulcer was 
thought to be doubtful. A very similar case was recorded by 
Eehn (7) in an infant aged twenty-one months with tuberculosis, 

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where microscopic examiDation of the ulcer showed no evidence of 

In addition to the cases mentioned above I have been able to 
find onlj four cases (8) recorded of tubercular gastric ulcer in 
children ; two of these were verified bj microscopic examination. 

As regards the age at which tubercular gastric ulcer is most 
often found, it seems probable from the number of cases recorded 
in children that it is less rare in children than in the adult; 
and it occurs probably more often in infancy and in the earlier 
years of childhood than in later childhood. Pour out of my five 
cases were in children under the age of four years, one at the age 
of ten months, and Holt mentions that four out of his five cases of 
gastric ulcer in tuberculosis were in infants. 

Four out of my five cases were males. One can hardly attach any 
significance to such small numbers, but so far as they go they 
agree with the observation of Billiet and Barthez, who found that 
fourteen out of twenty-one were males. This predominance of the 
male sex may perhaps be related to the frequency with which 
tubercular ulcer of the stomach is associated with tubercular peri- 
tonitis, a condition which statistics show to be considerably more 
frequent in males than in females. 

Vomiting was present in all my cases, but as tubercular perito- 
nitis was present in four of them, and tubercular meningitis in the 
remaining one, no special importance could be attached to the 
vomiting as a symptom of the ulceration. Tenderness in the ab- 
domen for the same reason had no special significance. It could 
not, indeed, be said that there was any clinical evidence of the 
gastric ulcer in these cases, and this absence of symptoms is 
noticeable in the other recorded cases, with the exception of one 
recorded by Bignon (8), in which a girl, aged six and a half years, 
with general tuberculosis, had fatal hsematemesis from a gastric 
ulcer thought to be tubercular, and one recorded by Cazin (quoted 
by Holt, loc. cit.), in which a tubercular ulcer caused perforation 
of the stomach and acute peritonitis. In Case 4 recorded here, one 
of the ulcers had perforated the stomach, but without producing 
peritonitis, as the opening was blocked by dense adhesions between 
the stomach and the surrounding structures. In such a case it is 
difficult to be sure whether the perforation was from within or from 
without. In some cases, as in that recorded by Dr. Newton Pitt, 
in an adult, and another mentioned by Dr. Wilson Pox (9), a caseous 


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gland or deposit outside the stomacli becomes adherent to the 
outer surface of the stomach and perforates by ulceration from 
without : and in the specimen shown from Case 4 it will be seen 
that there are numerous caseous deposits in the adhesions on the 
outer surface, one of which might in this way have produced the 
perforation, but the presence in this case of another ulcer which 
has not yet reached the outer surface is opposed to this view. 

The position of the ulcer in all the five cases recorded here was 
on or near the lesser curvature, and in all it was on the posterior 
wall, but in one there was also ulceration on the anterior wall. 
Eilliet and Bartbez (loc. cit.), on the contrary, state that these 
ulcers are usually situated on the greater curvature. 

In four out of my five cases there was tubercular peritonitis, and 
in all tlie intestine showed more or less ulceration ; but it is note- 
worthy that the ulceration in the intestine was only slight in two 
of them, while in one it was particularly noted that the ulceration 
was limited to the neighbourhood of the ileo-caecal valve. It would 
appear, therefore, that the occurrence of tubercular ulceration of 
the stomach bears no relation to the extent of ulcemtion of the 

In the microscopic specimens shown from Cases 1, 2, and 3, the 
tubercular process seems to have started in the submucous tissue, 
and the mucosa can be seen to be undermined by the caseous area 
M the edge of the ulcer. 

It is diflScult to be certain whether the tubercular infection of 
the wall of the stomach occurs from without or from within. In 
the three cases examined microscopically there is certainly no 
4irect extension from the peritoneal surface, but, as already men- 
tioned, this probably occurs in some cases. In others, no doubt, 
the infection is from within, t. e, from the contents of the stomach, 
especially tubercular material, coughed up from the lungs and then 
.swallowed ; and it may be that peritoneal adhesions by impeding 
the movements of the stomach predispose to such a mode of infec- 
tion. In others, again, as in Case 2, where the ulcer occurs in as- 
sociation with acute miliary tuberculosis, it is probable that the 
deposit of miliary tubercle in the wall of the stomach is simply 
part of a general blood infection. 

In all the five cases recorded here, as in those which I have been 
able to find recorded elsewhere, there was extensive tuberculosis 
in many organs of the body. Moreover, while the tubercular 

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lesions elsewhere were advanced, the ulcers in the stomach have 
usuallj been quite small, a fact which suggests that the gastric 
ulceration is quite a secondary and a late phenomenon. It seems 
at any rate clear in these cases that the gastric ulcer cannot be re- 
garded as the primary channel of infection. 


1. Gerhardt's * Handbnch der Einderkrankheit./ iy, 2, 448. 

2. Steiner u. NeureuUer.—* Prager Vierteljahresschrifl;/ 1866, Bd. ii. 

3. Milliet and Barthez.—* Maladies des enfants.' Paris, 1843, iii, 437. 

4. jffb^f.— 'Diseases of Infancy and Childhood.' London, 1897, p. 804. 
6. * Path. Soc. Trans.,* xxxix, p. 107 (Pitt), and xlv, p. 73 (Habershon). 

6. JBarlow, — ' Path. Soc Trans.,* xxxviii, p. 141. 

7. J2«Afi.— « Jahrb. fdr Enderheilk.,* 1874, p. 19. 

8. Biffnon,^* BnlL de la Soc. Anat.* Paris, 1853, vi, 211. 

9. WtUon Fox, — ' Reynold8*s System of Medicine,* vol. ii. 

Other references are : Barbacci, * Lo Sperimentale,' Ixv, 1890 (a good epitome 
of literatare); Talamon, *ProgrU m^cal,' 1879, iii, 46; Bednar, 'Erankheit 
der Nengebor. u. Singling.,* t. cxvi ; Blumer, ' Albany Med. Annual,* March, 
1898 (thirty cases collected from literature). 

May 2nd, 1899. 

12. A specimen of tubercular ulceration of the stomach from a 
child, {Card specimen.) 

By T. D. Lister, M.D. 

/\n the posterior wall of the stomach the mucous membrane 
v shows numerous tubercular ulcers of various sizes. The 
largest is situated at the cardiac end and is about a quarter of an 
inch long, with deeply undermined edges. Close to it is another, 
about one eighth of an inch long, and scattered along the course 
of the vessels are other smaller ulcers, some being mere raised 
nodules with a tiny central perforation. In this specimen the 
ulcers are all situated in close relation to the vessels. This was 
more readily seen in the recent state, when the thick or nodular 
edges of the ulcers and their central translucent bases were very 

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obvious on holding the well-washed organ up to the light spread 
out on a piece of glass or stretched in the fingers, all the ulcers 
being seen close to the larger arborescent arteries. 

Microscopically the bases of two of the ulcers showed giant-cells, 
two of the smaller ulcers having been excised for the purpose, and 
the holes sutured as is seen in the naked-eye specimen. 

Abstract of case. — Timothy D — , aged 1 year 10 months, was 
admitted to the East London Hospital for Children, on April 21st, 
1897, with a history of six months' diarrhoea and fourteen days' 
cough and dyspnoea. The patient was very wasted, presented the 
physical signs of broncho-pneumonia, and died soon after admission. 

At the autopsy the condition already described was found. The 
intestines showed very numerous tubercular ulcers, some of very 
considerable size, scattered through the intestinal tract. The liver 
exhibited very numerous tubercles, some as large as peas, contain- 
ing deeply bile-stained, caseous debris. The mesenteric glands 
were caseous, and some were breaking down centrally. The lungs 
were full of grey tubercles, the mediastinal glands were large and 
caseous, and there were numerous subcapsular and interstitial grey 
tubercles in the spleen and kidneys. 

Comment, — The occurrence of specific ulceration of the stomach in 
acute generalised tuberculosis would seem to be less uncommon than 
is generally thought, though the smaller ulcers are readily over- 
looked. In thirty cases examined by my predecessor (Dr. Eake) 
and his locum tenens at the East London Hospital for Children one 
example was found, and the specimen was preserved. During the 
last two years, my attention having been drawn to this subject by 
that specimen, I have examined forty-two cases of acute tubercu- 
losis in children, and have found ulceration of the stomach in four. 
The five cases of which I have a record are as follows : 

(1) Dr. Rake's specimen, Maud H — , aged one year 9 months. 
Large ulcers on posterior wall. 

(2) The case here described, Timothy D — , 1 year 10 months. 
Small ulcers on posterior wall. 

(3) (P. M. Bk., I, 615), Mary C— , 2 years. One small ulcer on 
anterior wall. 

(4) (P. M. Bk., I, 809), Edward S— , 9 months. Six ulcers, four 
close together on anterior wall. 

(5) (P. M. Bk., II, 94). Daisy W— , 4 months. One small ulcer 
on posterior wall near pylorus. 

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No. 5 was the only doubtful case, and was confirmed microscopic- 
ally as well as (2) the slides being shown. 

The history of the present case and the advanced riiorbid 
appearances found in the gastro-intestinal tract and liver (as com- 
pared with those elsewhere, which seemed to be of a later date) 
would seem to point fairly definitely to a tubercular infection by 
way of the digestive organs. 


CoaU, — * Glasgow Med. Jonrn.,' xxvi, 1886. 

Blackader, quoted in ' Starr's Text-book,' i, 452, says, " Tubercular ulcers are 

often multiple." 
Steiner and Neureuther, quoted by Rebn, ' Jabrb. f. Kinderb.,' 1874, S. 1 (4 

cases in 802). 
Widtrhoftr, quoted in * Gerbardt's Handb.,' vol. iv, S. 444 (2 cases in 418). 
Milliet and Barthez,--* Traits des Malad. de I'enfance,' vol. iii, 1262 (21 in 141 

Hamilton,—* J. Hopkins Hosp. Bulletin,' April, 1897 (8 cases). 
Kundrat, — * Gerbardt's Handb. d. Einderk.,' iv. 
Serafini,—* Ann. Clin. dell. Ospedal. degl' Incurab.,' Naples, 1888. 
JAtten,—" Tuberc. Ulcer, of Stomscb," Virch. Arch. Ixvii, 1876. 
BlMmer.^* kWiBJiy Med. Ann.,' March, 1898 (18 cases: 14 males; 24 cases, 

multiple in 12). 
Senkel.—' Gas. hebdom. de M^. et de Chir./ March 81st» 1898 (bacteria in 

ulcers, streptococci). 

May I6th, 1899. 

18. Myoma of the stomach. {Card specimen.) 
By Alexander G. E. Touleeton. 

THE specimen was met with in the course of an operation on the 
gall-bladder, by Mr. Bland Sutton, in a woman aged 60. 
The tumour was situated in the posterior wall of the stomach, not 
▼ery far from the pylorus, and was removed by an incision through 
the mucous membrane after the viscus had been opened. The 
tumour is round in shape, and measures 2'3 cm. in diameter. It 

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is of a firm consistence and white in colour. Histologically it 
consists of unstriped muscle, without any admixture of fibrous 
tissue. February 21«<, 1899. 

14. Congenital hypertrophy of the pylorus. 
By Gboegb F. Still, M.D. 

CONGENITAL hypertrophy of the pylorus is so obscure in its 
pathology that any addition to the number of cases on 
record is perhaps worth making, in the hope that some light may 
be thrown on this condition. It is rather with this object of 
increasing the available facts than with the intention of propound- 
ing any new theory of causation that I venture to record here 
three cases which I have examined poet mortem at the Hospital for 
Sick Children, Great Ormond Street. 

Case 1.— Richard W — , aged 12^ weeks at death. A fine baby 
at birth, and thought to be healthy until the end of the sixth week 
of life, when he began to vomit. Before this, however, the child 
used to regurgitate some of its feeds every day, but mother thought 
this was natural. Was fed on breast only until nine weeks old. 
Since six weeks old wasting, vomiting after nearly every feed^ 
apparently some pain in abdomen soon after taking breast. 

On admission to hospital child extremely weak and wasted, with 
depressed f ontanelle, and muco-pus on cornea ; he improved, how- 
ever, in spite of several convulsions and daily vomiting, usually of 
very small amounts and less than the food taken. Several kinds 
of food were tried in various amounts and at various intervals, but 
with little or no effect on the vomiting ; partial rectal feeding was 
also tried, but with little advantage as the bowels worked fre- 
quently. There was no constipation. The temperature during 
the last ten days of life was continuously subnormal. Abdomen 
was flat and supple, and during the last few days before death a 
tumour suggesting a thickened pylorus was felt in the right 
hypochondrium. Death occurred two and a half weeks after 

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Post-mortem. — ^The stomach was normal in position and shape. 
It measured from cardiac end to pylorus 9*5 cm., from lesser curve 
to greater 6 cm., and was therefore not obviously larger than 
normal. The whole of the stomach wall was thicker than normal, 
and the thickening of the muscular coat became very marked about 
4*5 cm. on the cardiac side of the pylorus, and increased gradually 
up to the pylorus. 

The most striking change was the great thickening of the 
pylorus, which formed an almost tumour-like enlargement of that 
portion of the stomach ; it felt, indeed, very like a pylorus affected 
with scirrhus. The lumen of the pylorus was more than 3'5 mm. ; 
as it admitted easily a probe with that diameter, it could hardly 
have been less than 4 mm. The wall of the pylorus on section was 
7 mm. thick, the muscular part being 5 mm., and the mucosa and 
submucosa together 2 mm. The stomach wall about 4 cm. from 
the pylorus was 3 mm. thick, and at the cardiac end was 2 mm. 
thick. ■ The thickening of the pylorus terminated abruptly on the 
duodenal side, the thin wall of the duodenum contrasting markedly 
with the hypertrophied pylorus. There was no ulceration of the 
mucous membrane, but ^ome post-mortem digestion had commenced 
in the gastric mucosa. The oesophagus seemed normal. 

The only other congenital abnormality found was that the 
second and third toes were webbed together in both feet nearly up 
to the proximal interphalangeal joint, but such webbing of these 
particular toes is so common that no great importance can be 
attached to it. 

Case 2. — Albert L—, set. 14 weeks at death. Fine child when 
bom, and seemed perfectly healthy till six weeks old ; before this 
there was not the slightest regurgitation of food ; then began to 
vomit, usually large quantities after intervals of several hours. 
Constipation troublesome since onset of vomiting. Breast feeding, 
with addition of some condensed milk owing to large appetite, 
until eight weeks old ; then various methods of feeding were tried, 
sometimes diminishing the vomiting for a time, but not perma- 

The mother herself noticed peristalsis of the stomach when the 
child was three months old. 

On admission to hospital, child much wasted, abdomen slightly 
full, marked peristalsis, evidently of stomach, from left to right. 

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visible iii epigastrium ; apparently no pain. Peristalsis increased 
during the last two weeks of life, and on the day before death the 
hard pylorus could be very distinctly felt in the right hypochon- 
drium. Temperature was subnormal, there was almost daily 
vomiting, the bowels were regular; the child became gradually 
weaker, and died after being in the hospital fifteen days. 

Post-mortem, — The stomach was slightly but distinctly dilated, 
and there was evident hypertrophy of its wall. The position of 
both stomach and pylorus seemed to be normal. Towards the 
pylorus the thickening of the wall was more marked, and increased 
gradually up to the pylorus, which was considerably thickened 
and hard, almost as if cartilaginous, to the touch. The circum- 
ference of pylorus was 4*75 cm., length 2*6 cm. The wall was 
5 mm. thick, and the thickening was evidently muscular ; the 
mucous membrane, which was thrown into longitudinal folds by the 
contraction of the pylorus, was not thicker than normal. The 
lumen was perfectly patent, and was over 8*5 mm. in diameter. 

The (esophagus was probably thicker than normal, the muscular 
layer being increased. The mucous membrane was normal. The 
duodenum was normal. 

No other congenital abnormalities were found, except that the 
skull was markedly asymmetrical. 

Case 8. — John N — , set. 14 weeks at death. Was thought to be 
quite healthy till three weeks old ; the mother said there was no 
vomiting before this, but on further questioning said that there 
had been some regurgitation of food which was thought to be 
natural, since the child was seven days old. Began to vomit 
almost all his food when three weeks old, and this had continued 
ever since, with slight tompoi*ary improvement each time the food 
was altered. At first the vomit consisted of food only, but after a 
few weeks it contained ** phlegm and slime," and occasionally a 
streak of blood. The child was suckled one week, and then had 
milk with barley-water, and then various foods in the hope of 
controlling the vomiting. The bowels were costive ; there had 
never seemed to be any abdominal pain, but the child cried often 
just after vomiting. Latterly there had been wasting, and the 
child seemed very collapsed sometimes. There had been one con- 
vulsion at nine weeks old. 

On admission to hospital, child emaciated, with eyes sunken and 

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fontaDelle depressed. There was visible peristalsis of the stomach 
from left to right, and the lower edge of the stomach was about 
three quarters of an inch above the umbilicus. A hard tumour 
could be distinctly felt in the region of the pylorus. Vomiting 
persisted after almost every feed ; the temperature was subnormal. 
There was a marked diminution of the vomiting when nasal feeding 
was begun five days before death, but the child was now extremely 
feeble, the bowels had become loose, and death occurred on the 
tenth day after admission. 

Post-mortem. — The stomach and pylorus seemed to be in the 
normal position. The stomach was little if at all dilated ; its wall 
was thickened, the thickening being evidently muscular and 
increasing towards the pylorus ; it contained some partially 
digested milk with a good deal of mucus. The pylorus could be 
felt distinctly through the abdominal wall before opening the 
body, and when exposed felt quite like a pylorus infiltrated with 
firm malignant growth, but on section it was evident that the 
thickening was muscular, and that the increase of muscle was 
mainly in the circular layer. The diameter of the pylorus was 1*4 
cm., its length was 2*4 cm. ; the muscular portion of the wall was 
4*5 mm. thick; its lumen was normal, admitting a probe with 
diameter 3*5 mm. easily. The condition of the mucous membrane 
was uncertain, as some post-mortem digestion had occurred. 

The cardiac orifice was normally patent, but the oesophagus, 
especially at its lower end, was distinctly hypertrophied. The 
upper few inches of duodenum, compared with that of an infant 
eleven months old, seemed to be a little thicker than normal. 

The right kidney showed considerable dilatation of the pelvis, 
and the upper two inches of the ureter were also slightly dilated ; 
no cause whatever for the hydronephrosis could be found. The 
bladder was normal, and the other kidney was normal. 

The microscopic appearances of the pylorus in these three cases 
were so similar that one description may well serve for them all. 
The increase in thickness is almost if not entirely limited to the 
muscular coat, and the part of the muscular coat in which the 
increase has chiefly occurred is the circular layer. From the 
actual micrometric measurements given below it will be seen that 
the longitudinal layer was actually within the limits of normal 
thickness in Cases 1 and 2, while in Case 3 it was distinctly beyond 

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the normal limit, though here also the main increase is in the 
circular coat. 

There is no definite increase of fibrous tissue, but the bundles of 
muscle-fibres in the circular layer are perhaps rather more dis- 
tinctly marked off bj the fibrous trabeculee than is common in the 
normal pylorus. 

The submucosa in Cases 1 and 2 was normal in thickness ; in 
Case 3 it was about twice the normal thickness. I have been 
unable to satisfy myself that there was any particidar '* condensa- 
tion" of the fibrous tissue here. 

The mucosa was normal in thickness, so far as could be ascer- 
tained, in all three cases. There was no evidence of inflammatory 
infiltration past or present. 

The serous layer was not thickened in any of the cases. 

In considering the morbid anatomy and pathology of congenital 
hypertrophy of the pylorus, it seemed to me of importance that a 
fuller study of the normal pylorus should be made ; for so far as 
I have been able to ascertain, there is only one published record of 
accurate measurements of the several layers of the pylorus in the 
normal infantile stomach,^ and as the writer records only one 
observation, there is very little material on which to base any 
statements of relative hypertrophy of the various layers. I have, 
therefore, examined carefully and made micrometric measurements 
of the pylorus in eight infants within the first year, and these I 
have tabulated below. 

The specimens were hardened in Muller's fluid and cut with a 
freezing microtome in the ordinary way by my friend Dr. Crowley, 
now of Bradford. The method of preparation, therefore, entailed 
some shrinkage, and consequently the measurements must not be 
compared with the fresh specimen ; but as all the sections were 
prepared in the same way, they are of some value both for com- 
parison with each other and with the hypertrophied pylorus pre- 
pared in the same way. 

Prom these measurements the following points are evident : — 
First, that there is considerable variation in the thickness of the 
wall of the normal pylorus. In making a large number of post' 
mortems on infants one has been struck with this variation. It is 
by no means uncommon to find a pylorus considerably thicker and 
^ Grau, ' Jahrb. f. Einderbeilk.,' xliii, i, 118. 

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firmer than the average, in cases where there has been nothing to 
suggest anything wrong with the stomach during life. And such 
variation is, I think, not merely a question of muscular contraction 
or relaxation, there is some actual increase of muscle tissue. This 
conclusion from naked-eye observations is confii-med by the 
measurements given below ; thus in one child, aged 5 months, the 
wall of the pylorus was 1*7 mm. thick, while in another of the same 
age it was 2*6 mm. In one child of 10 months tbe whole thickness 
was 2*4 mm., in another at the same age it was 1*5 mm. In view of 
this normal variation (and I regret that I cannot bring forward 
larger statistics, from which we might deduce the limits of normal 
thickness), it is evident that slight degrees of hypertrophy are very 
difficult to determine, and must be received with extreme caution. 

Secondly, the variation in the thickness of the normal pylorus 
is mainly due to a variation in the thickness of the circular muscle. 
For instance, in one infant aged 4 weeks the thickness of the 
pylorus was at least 1*8 mm., while in a child aged 10 months it 
was only 15 mm. A comparison of these two cases showed that 
while the longitudinal layer was almost exactly equal in them, the 
circular was 1*05 mm. in the thicker pylorus, and only '66 mm. in 
the other, so that almost the whole difference in the thickness was 
due to difference in the circular muscle. 

Thirdly, there is very little variation in the thickness of the 
submucosa, but occasionally even this seems to be considerably 
thicker than the average. 

A further point in the anatomy of the normal pylorus during 
infancy seems to want investigation before discussing the 
pathology of congenital hypertrophy of the pylorus. I mean the 
size of the normal lumen. My own observations on this point 
are not sufficiently numerous to be of much value, but so far as 
they go they show that a lumen of 3*5 to 4 mm. in diameter is 
not below the normal limit for the pylorus during the first year, 
as seen post mortem. This measurement is, of course, that obtained 
by measuring without any stretching of the pylorus, and was made 
in my own observations, by finding the largest probe or glass rod 
of known diameter which would pass through the pylorus quite 
easily, or with no more pressure than its own weight would afford. 

Another less important detail in the anatomy of this part is 
perhaps worth mentioning, namely, the appearance of the pylorus 
as seen from the stomach, and as seen from the duodenum. 

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Particular mention has been made by several writers of the 
funuel-like shape of the pylorus on the stomach side, and of its 
likeness to the lower end of the cervix uteri on the duodenal side, 
in cases of congenital hypertrophy of the pylorus. It is to be 
remembered, however, that such an appearance is not peculiar 
to congenital hypertrophy of the pylorus ; indeed, it is not 
pathological at all, for exactly similar appearances, though to 
A less degree, are noticeable in the normal stomach, and are par- 
ticularly well seen in the cases where, as already mentioned, the 
pylonis happens to be thicker than usual. 

The muscular layer is seen in the normal stomach to thicken 
gradually towards the pylorus, the thickening beginning 2 to 3 cm. 
on the stomach side of the pylorus ; in the pylorus itself the 
thickening continues, but less rapidly, up to the duodenal opening, 
where there is a sudden increase of thickness due to the presence of 
additional bundles of circular fibres. Here the pyloric thickening 
ceases abruptly, and the thin duodenal wall begins ; consequently, 
even in a normal stomach, the cervix-like appearance is produced. 

In view of this gradual increase of thickness even in the pylorus 
itself, it is unfortunate that in several of the recorded cases of 
congenital hypertrophy of the pylorus no mention is made of the 
position at which the pylorus was measured. It will be seen from 
the normal measurements given below that there may be as much 
as 1*1 mm. difference between the thickness of the wall at the 
duodenal end of the pylorus and the thickness at a point about 
half a centimetre nearer the stomach — a difference which would be 
even greater in the fresh specimen. With these preliminary 
remarks I pass on to the consideration of congenital hypertrophy 
of the pylorus. 

Pour views have been held of the pathology of that condition : 

(1) That the thickening of the pylorus occurs entirely in extra* 
uterine life, and is the result of spasm from some irritant in the 
stomach (Siemon-Dawosky). 

(2) That the increase in thickness of the pylorus is the result 
of a developmental hyperplasia, " a vice of developmental growth " 
(Adams re Peden's case, * Glasgow Med. Journ.,' 1889). 

(3) That a primary narrowness of lumen, a congenital stenosis, is 
followed by compensatory hypertrophy of the stomach, especially the 
pylorus (Finkelstein, De Bruyn Kops, Meltzer, Landerer,Maier). 

(4) That there is " a functional disorder of the nerves of the 

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8tx>macli and pylorus leading to ill-co-ordiDated, and therefore 
antagonistic action of their muscular aritingements ; " and that 
this functional disorder begins in uiero (J. Thomson). 

The first theory has at any rate one point in its favour, that it is 
applicable to, and is, I believe, the accepted explanation of, the 
remarkably similar cases met with in adults. These cases of 
••idiopathic hypertrophic stenosis " in adults are due, it is thought, 
to spasm of the pylorus produced in some cases by superabundance 
of acid in the contents of the stomach, in others by the presence 
of an ulcer in the pyloric region, or some such irritant. No such 
cause of irritation has been demonstrated, however, in the infantile 
cases ; and, moreover, it seems extremely unlikely that these cases 
have their origin during extra-uterine life. 

The strongest objection to an extra-uterine origin is the improba- 
bility, perhaps impossibility, of so great a hypertrophy occurring 
within the short period of extra-uterine life in some of these cases. 
Thus in one case life only lasted twenty-one days, in two others 
twenty-eight days and thirty days respectively, and yet in each of 
these cases the hypertrophy was great. Moreover the degree of 
hypertrophy does not correspond to the duration of life or of 

A further point on which observations are much wanted is the 
date at which the pylorus first becomes palpable. There can, I 
think, be no doubt that with careful palpation the pylorus would 
be felt in a much larger proportion of cases than is recorded. The 
diagnosis has been so often made for the first time post mortem, 
that no special attention has been paid to this point during life, so 
that it is hardly fair to draw any conclusions from such records. 
I have myself seen four cases in which the pylorus was felt during 
life, and Dr. Barlow telle me of another that was under his care. 
If, however, from subsequent observations it can be shown that 
the pylorus is palpable at birth, then assuming, as I think we may, 
that a pylorus which can be felt is an enlarged pylorus, we should 
have positive proof that the condition was intra- uterine in its origin.^ 
The recorded facts at present are not conclusive ; the earliest date 
recorded in five cases in which it has been felt was the twenty- 
seventh day ; ^ the others were much later, none being earlier than 
the fourth month. So far as the facts go, they seem to show that 
the pylorus does not reach such a thickness as to be palpable 

^ J. Tborason, ' Scottish Med. and Surg. Journ.,' June, 1897 (Bibliogprapby). 

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clinically until several weeks or months after birth ; it would seem, 
therefore, that the hypertrophy is, at any rate in part, an extra- 
uterine development. 

The fact that vomiting begins often within the first few days of 
life has been adduced as evidence of a congenital affection, and 
perhaps, considered in connection with the other points in favour 
of this view, it may be of some value ; but in itself it is of little 
importance, for there is nothing to show that this early vomiting 
is necessarily the result of hypertrophy of the pylorus, or to 
distinguish it from vomiting due to any other cause ; indeed, it 
might just as reasonably be adduced as evidence of exti*a-utenne 
gastric irritation producing subsequent hypertrophy. 

The second view, which assumes a primary congenital stenosis 
as the cause of the hypertrophy, hardly needs consideration. The 
observations on the size of the lumen of the pylorus mentioned 
above, show that the measurements given in several recorded cases 
of hypertrophy are well within the normal limits, perhaps even 
above the average. The stenosis is the result of muscular con- 
traction during life ; in other words, it is the result, not the cause 
of the hypertrophy. 

It may well be, however, that there is another quite separate 
group of cases, such as those described by Maier ^ and Landerer,^ 
and perhaps the second case described by Dr. Ashby (* Archives of 
PflBdiatrics,* 1897, p. 498), in which a congenital narrowness of lumen 
of the pylorus, especially at its duodenal end, acting as a stricture, 
produces some general hypertrophy of the stomach including the 
pylorus ; but it would seem that in such cases the hypertrophy of 
the pylorus is a much less striking feature than in those under 

Developmental hyperplasia, the third theory, is not altogether 
without support. The observations which I have recorded above 
show that there is considerable variation in the thickness of the 
normal pylorus, and the maximum limit of the normal comes very 
close to the minimum limit of the hypertrophied pylorus. 

Further, the differences in the normal thickness, as I have shown, 

are mainly in the circular muscle, and this is notably true of the 

hypertrophic cases also. It might well be suggested, therefore, 

that the so-called hypertrophic pylorus might be merely one end 

» ' Virchow's Archly,' Bd. en, Hft. 3, p. 418. 

" 'TJeber angeb. Steno«e des Pylorns,* Dissert., Tubingen, 1878. 

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of the scale of developmental variation, and that as a result of 
this unusual muscular development the wall of the pylorus is 
unusuallj rigid, and so unable to dilate f uUj, and hence hyper- 
trophy and dilatation of the stomach, and all the usual train of 
symptoms. Such a theory, however, is completely negatived if it 
can be shown, as seems probable, that the pylorus becomes 
palpable only some weeks or mouths after birth. 

Moreover there is some evidence that the condition is a recoverable 
one. Finkelstein^ and Senator ^ have recorded such cases, and 
Dr. Barlow tells me of one where recovery seemed to have occurred. 
If this be confirmed by further observation, it would go a long way 
towards disproving any theory which assumed the presence of a 
maLformation in these cases. A further objection is, I think, the 
fact that such a theory necessitates an entirely different pathology 
for the hypertrophic pylorus of adult life. 

The last theory which needs to be considered is that put forward 
by Dr. John Thomson, of a functional disturbance of the nervous 
mechanism of the stomach, occurring in utero (' Edinb. Hosp. 
Rep.,' vol. iv, p. 116 and loc. cit,). As already pointed out, the 
balance of evidence is strongly in favour of this condition being 
intra-uterine in its origin ; and this being so, the choice seems to 
rest between an unexplained vice of developmental growth and 
hypertrophy from increased work. The objections to the develop- 
mental view have already been stated. The suggestion that a 
defect of nervous co-ordination leads to antagonistic action, and so 
to hypertrophy of the muscles of the stomach, is at any rate in 
accordance with the common experience that elsewhere hyper- 
trophy of muscle results from increase of work. To this extent 
also the explanation would agree with that accepted for the adult 
cases of hypertrophic pylorus, in which hypertrophy is thought to 
be due to spasmodic action of the pylorus, the result of some irri- 
tation. In the infantile cases, however, there is no evidence of 
any irritant, and for this reason Dr. Thomson has suggested that 
the spasmodic action may be due to a functional disturbance. 

The question therefore arises, whether there is any evidence to 
show that functional spasm may occur here, and whether it may 
occur during intra-uterine life. 

Apart from the inherent probability of such an occurrence there 

1 ' Jahrb. far Kinderheilk./ Bd. xliii, p. 105. 
^ ' Berlin, klin. Wochensohr./ January, 1897. 

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are cases which seem to point in this direction. Cases have been 
recorded in which the oesophagus has been found hypertrophied, 
the thickening ceasing abruptly at the cardiac orifice where there 
was no evidence whatever of stenosis. Dr. Eolieston has recorded 
such a case in the * Transactions ' of this Society (vol. xlvii), and 
has suggested that the cause was spasm of the cardiac orifice. If 
such be, as seems possible, the correct explanation of these cases, 
we have in them a close analogy for functional spasm of the 

It is very difficult, however, to prove that such a spasm may 
occur in utero. Dr. Thomson records the case of a male infant 
aged seventeen days, who had enoimous dilatation of both ureters, 
very great hypertrophy with dilatation of the bladder, and no dis- 
coverable obstruction in the course of the urethra, and suggests 
that in such cases the whole condition may be the result of dis- 
ordered co-ordination. 

It has been suggested also that some irregularity of nervous 
mechanism producing irregular contraction of the intestine, or even 
spasmodic contraction of the sphincter ani, may possibly underlie 
some of the cases of congenital dilatation of the colon. 

It will be seen, therefore, that although no actual proof can be 
produced, there are cases which suggest that a functional disturb- 
ance may occur in such a part, and moreover may occur in utero. 
Such an explanation seems on the whole to be the most rational 
that has yet been offered to explain these cases of congenital hyper- 
trophy of the pylorus ; but there is one point in the theory put 
forward by Dr. Thomson which seems to require some emphasis in 
the light of further observations. He considers it most likely that 
a derangement probably from faulty development of the nervous 
mechanism may be the cause of the over-action of the pylorus. 

This faulty development, which he elsewhere speaks of as 
" delayed or imperfect development," must be regarded as a 
potentially transient condition, not a permanent developmental 
fault even of function ; for there is, as I have already mentioned, 
increasing evidence that infants with this condition do occasionally 
recover. And there is, I think, no difficulty in such a supposition ; 
co-ordination of the voluntary muscular actions is only gradually 
acquired, and even the not altogether voluntary action of the 
respiratory muscles is but imperfectly co-ordinated in infancy; 
moreover tlie time at which perfect co-ordination is acquired varies 

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within certain limits ; it may well be that in some cases, at any 
rate, the establishment of perfect co-ordination in the involuntary 
muscular action is also delayed, and so antagonistic action occurs 
leading to hypei-trophy. 

Other references are — Siemon-Dawotky, * Caspar's Wochenschrift/ 1842, No. 
7, p. 106 ; De Bruyn Kopt, * Nederlandsch Tijdschrif t voor Geiiet^skunde/ 1896> 
No. 26, and *Brit. Med. Journ.,' 1897, i. Epitome 103; Meltter, 'Medical 
Record,* August, 1898 (bibliography) ; Molleston and Hayne, * Brit. Med. 
Journ.,' 1898, i, 1070; Caufley, ' Med.-Chir. Trans./ 1898, p. 41 ffull biblio- 

February 7th, 1899. 

15. Congenital hypertrophy of the pylorus, {Card specimen,) 
By H. MoBLEY Fletcher, M.D. 

THE pylonis, stomach, and part of the oesophagus of an infants 
presented to the museum of St. Bartholomew's Hospital by 
Dr. J. Eaglan Thomas, of Exeter. 

There is great hypertrophy of the muscular coat of the pylorus. 
The stomach is also thickened, and the oesophagus is dilated. The 
mucous membrane of the pylorus is congested and swollen. Micro- 
scopical examination showed nothing of the nature of any tumour^ 
the thickening being simply an overgrowth of the unstriped 
muscular tissue. This ceases quite suddenly on the distal side of 
the pylorus, but gradually tapers off towards the cardiac end of 
the stomach. 

From an infant aged seven weeks, quite healthy at birth. When 
three weeks old vomiting began, which continued in spite of all 
treatment until the child died of inanition. At the autopsy no 
cause for death could be discovered bejond the hypertrophied 
pyloms. This measured 2 inches in diameter, and felt very hard. 

February 7th, 1899. 

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16. Carcinoma of the cardiac orifice of the stomach. 
(Card specimen,) 


IlHBBB was a firm, raised growth surrouuding the cardiac orifice 
. and almost entirely limited to the stomach. There was no 
reason to think that it had begun in the lower end of the oeso* 
phagus and subsequently spread to the cardiac orifice. Micro- 
scopically it was a spheroidal-celled carcinoma, thus agreeing with 
the histological nature of carcinoma of the cardiac end of the 
stomach ; it did not show any sign of a transition from squamous- 
celled carcinoma, the characteiistic growth of the oesophagus. 
There was some dilatation of the oesophagus in its lower half. 
The specimen is brought forward to show that though Pagge's 
dictum that almost all the cases that have been set down as 
examples of carcinoma affecting the cardia have really been cases 
of carcinoma of the oesophagus spreading to the stomach is very 
often justified, it is not invariably supported even by the cases 
which a priori should be most likely to do so. These cases are 
those of carcinoma surrounding the cardiac oj-ifice, which are, one 
would think, much more likely to have spread from the oesophagus 
than those cases of carcinoma abutting on the cardiac orifice, but 
not passing completely round its circumference as in the present 
instance. It is noteworthy that Hale White, in his article on 
tumours of the stomach in AUbutt's * System of Medicine,' vol. iii, 
p. 664, comes to the conclusion, on the basis of Shaw and Perry's 
valuable statistics, that carcinoma limited to the cardiac end of 
the stomach arises there and may spread up to the oesophagus, 
and not vice versa as Pagge ^ supposed. I have seen cases of exten- 
sive carcinoma at the cardiac end of the stomach send out feelers 
of growth under the mucous membrane of the oesophagus on its 
last inch or two, but I believed until I came across this specimen 
that carcinoma of the margin of the cardiac orifice was of oeso- 
phageal rather than of gastric origin. The morbid anatomy and 
histological appearances of this specimen are strong evidence, 

» H. Fagge, * Principles and Practice of Medicine,' vol. ii, p. 146, Ist edit, 1886. 

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however, that carcinoma may attack the gastric surface of the 
cardiac orifice. 

The patient was under my care in St. Q-eorge's Hospital, and 
died with rapidly increasing weakness seven days after admission. 

For three months previously he had complained of debility, 
flatulence, and vomiting shortly after food. He was cachectic, and 
his skin was very inelastic and dry. He was fed per rectum to combat 
the vomiting, but his strength failed so rapidly that milky food 
was again tried by the mouth and vomiting returned. It was not 
thought that ho had any oesophageal obstruction, but the autopsy 
showed that there must have been. During life no tumour could 
be felt and no dilatation of the stomach made out, but he was 
thought to have malignant disease, possibly of the body of the 
stomach. February 7th, 1899. 

17. Carcinoma of the cardiac end of the stomach. (Card 

By Arthur Voblcker, M.D. 

(1a8e 1. — The stomach is not dilated. At the cardiac end is 
J a mass of new growth 3 inches in diameter, which does not 
involve the oesophagus. The growth is a malignant adenoma. The 
left lobe of the liver is adherent to the growth. 

Metastatic deposits were present in the liver, lungs, coeliac, 
mesenteric, and lumbar glands. Thrombosis of inferior vena cava. 
From a woman aged 42, who died in the Middlesex Hospital. 

Case 2. — The cardiac end of the stomach on both its anterior 
and posterior walls is the seat of a new growth which has destroyed 
the stomach wall and invaded the liver and pancreas. The lower 
end of the oesophagus is free from growth, except that some strands 
of new growth can be seen running upwards in its long axis. 

Duration of symptoms (pain and vomiting) eighteen weeks. 

From a man aged 61, who was admitted under the care of 
Dr. Coupland to the Middlesex Hospital. 

February 7th, 1899. 

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18. Spheroidal'Cell carcinoma of stomach involving the 
cesophaffus, {Card specimen.) 

By W. S. Lazarus-Bablow, M.D. 

THB specimen was taken from the body of a man, aged 66 years, 
who suflfered. from chronic renal fibrosis and its cardiac 
sequels, as well as from malignant disease. During his stay in 
hospital the renal symptoms were more pronounced than those due 
to the stomach. The only symptoms certainly referrible to the 
latter were emaciation and dyspepsia, with vomiting and heema- 

At the autopsy it was found that the stomach, so far as concerns 
the lesser curvature and the greater portion of the anterior and 
posterior walls, was the seat of a mass of new growth, which has 
obviously commenced at the cardiac end of the stomach, where the 
growth had degenerated and formed a foul ulcer about the size of 
a five-shilling piece. The greater curvature was free from growth. 
The oesophagus also shared in the growth ; at the gastric end is 
was thickened, and composed of a material which grated on section 
with the kuife. Above, it was the seat of innumerable nodules 
extending right up to the pharynx. Most of the nodules were 
collected into three lines running in the long axis of the tube on 
its anterior surface, and corresponding to the course of lymphatic 
vessels. In two or three places the masses had broken down and 
formed ulcers about the size of a threepenny piece. The mass 
described must be regarded as single, for there was no line of 
demarcation between the gastric and the oesophageal portions of 
the growth. Secondary nodules, strictly so called, were chiefly 
found in the lumbar glands, which were greatly enlarged. In the 
liver only one small nodule the size of a pea was found. The 
vessels at the hilum were contained in a hard but not extensive 
case of new growth that extended upwards from the main growth 
in the stomach. An extension from the main growth involved the 
left adrenal. A secondary nodule of gi'owth was present in the 
right adrenal. Nodules were also found in the left kidney and on 
the serous surface of the intestines close to the mesentery, but none 

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elsewhere in the body than in the sites mentioned. The primary 
growth in the stomach and oesophagus, as well as all the secondary 
growths, were definitely examples of spheroidal-cell carcinoma, 
differing from one another only in minor details dependent upon 
situation, rapidity of growth, &c. In the oesophagus the growth 
had greatly encroached upon the muscular bundles, and showed 
a general tendency for the cancerous cells to be arranged in long 

The interest of the case lies, firstly, in the fact that the gastric 
growth extends upwards into the oesophagus rather than down- 
wards into the stomach; secondly, that the growth obviously 
extends by way of the lymphatics ; and thirdly, in the extensive 
degree to which the oesophagus is affected. 

February 7th, 1899. 

1 9. Case of colloid carcinoma of the stomach. 
By E. G. Hebb, M.D. 

THE following case, though chiefly interesting from its clinical 
aspect, only an outline of which is subjoined, presents some 
pathological features worthy of record. 

A. G — , aged 30, office cleaner, was admitted to Westminster 
Hospital on August 4th, 1898, for vomiting, pain in upper part of 
abdomen, and emaciation. Family history unimportant. Lived 
in the country until twelve years old, when she came to London. 
Was married in 1893 ; had a miscarriage at three months. Was 
ill St. George's Infirmary, February, 1898, for rheumatism, since 
which has been troubled with pains and stiffness of the limbs. 
Has suffered from pains in the chest on and off for years. In 
April, 1898, she began to vomit after meals. The vomiting 
occurred ten minutes to thirty minutes after food, and has increased 
in severity. During the same period has also suffered from pain 
at the epigastrium and back before and after food, and lasting 
sometimes for hours. The pain was relieved by vomiting. There 
has been no heemateraesis. Is a sallow, thin little woman ; 
weight 5 St. 4 lbs. 8 oz. Besides the pain at epigastrium, <&c. 

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she complains of an no comfortable feeling in the throat on swallow- 
ing. There is some tenderness on palpation at the epigastric 
regioD. The abdomen is markedly retracted, and there is nothing 
abnormal to be felt or heard therein. There is no evidence of 
dilatation of the stomach or of anj tumour in the abdomen. 
Urine nil. Temperature normal throughout. Thorax nil. Tongue 
slightly fuiTed. Bowels constipated. The cervical lymphatic 
glands, especially on tho right side, are easily felt. There is lateral 
nystagmus. Examination of the oesophagus and stomach showed 
that there was no impediment to the passage of a large bougie in 
the former, and that the latter was small and tender. The amount 
was variable, but often Oj — Oiss. The vomit was a frothy, watery 
fluid, usually containing reddish-brown floccules, which much 
resembled semi-digested beef-tea. The reaction of the vomit was 
always markedly amphoteric, and on the occasions it was tested 
the absence of free HOI was noted. 

On October 11th the abdomen began to swell in the lower half, 
and by the 18th was generally distended with fluid. 

On the 28th she was transferred to the surgical wards, laparo- 
tomy was performed, and much clear ascitic fluid evacuated from 
the peritoneal sac. The patient died next day. 

The post mortem examination was made fifty-one hours after 
death. Body much emaciated, flaccid ; eyes sunken in orbits. 
Post-mortem decomposition commencing. Surgical wound four 
inches long in the middle line between pubes and umbilicus ; 
edges united by sutures and early adhesions. 

On opening the abdominal cavity the peritoneal sac is found to 
contain some pints of clear, thin, sauious fluid. There is no indica- 
tion of recent peritonitis. The intestines are drawn upwards, 
none lying in the pelvis. The peritoneum of mesentery, of pelvis, 
and of abdominal wall is somewhat thickened, white and opaque. 
The omentum is quite shrivelled. There is no subpentoneal 
thickening. The stomach measures 6 inches transversely. Its 
wall in the pyloric portion is hypertrophied, especially close to the 
ring, which is 1*5 inches in circumference. A great deal of the 
mucosa of the pyloric portion is absent (roughly estimated at 
about 2 square inches). The anterior surface is chiefly affected. At 
the margin of the ulcerated portion the mucosa is much swollen, 
soft, and red. 

The lower half of the oesophagus is dilated, its wall thickened, 

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aud the surface covered with white patches of thickened mucosa. 
Some few prevertebral lymphatic glands immediately above and 
below the diaphragm are enlarged, indurated, and buff-coloured 
on section. 

There are no peritoneal bands or adhesions. The intestines are 
normal. Liver 24 oz., nil; spleen 1| oz., nil; pancreas 2i oz., 
nil; kidneys 5^ oz., nil; adrenals nil; uterus nil; ovaries in- 
durated, puckered, about size of large almonds ; lungs nil ; heart 
4 J oz., nil; brain nil. 

Microscopical examination of the stomach shows the character- 
istic appearances of colloid degeneration of the mucosa with thick- 
ening of the submucous connective tissue. In the muscular 
coat are numerous collections of spheroidal cells, which in some 
parts have undergone the colloid change. In most places the cells 
have no definite disposition, and they form merely irregular collec- 
tions between the muscle bundles. Yet there are a few areas 
where there is evidence of arrangement in tubules, and these 
tubules are closely adjacent to the peritoneum. 

In the lymphatic glands the cells are larger and of a more 
polyhedral type. The nucleus is large ; in many places it is 
represented by a collection of granules — fragmented, in fact. There 
are also not a few large multinucleated cells with six or more 
nuclei. In the ovary, which presents the ordinary features of 
shrinking ovarian tissue, there are scattered throughout the stroma 
not a few cells which, though not absolutely identical in appearance 
with those in the stomach and lymphatic glands, present a striking 
resemblance to them. These are arranged in short tubules and 
cylinders. There is no evidence of colloid change either in lym- 
phatic gland or in ovary, but there is some hyaline fibrosis in both. 
In the lymphatic glands there are arese where the cells are in the 
granular condition of necrosis common in malignant growths. I 
was unable to detect the presence of a blastomycete. 

There are several points in the microscopical appearances to 
which allusion may be made, and which might serve as texts for dis- 
cussing some interesting and unsolved pathological problems. Such 
are the why and wherefore of the fiugmentation of the nucleus, 
the origin of the multinucleated cell as distinguished from the 
giant-cell, the reasons for the occurrence of the granular condition 
of necrosis, the causation of the colloid degeneration, and its rela- 
tion to other viscous states. It might afford a basis for attacking 

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the histological definitions of carcinoma and sarcoma, and of 
attacking them with success. But perhaps the chief point of 
interest lies in the relationship between the neoplastic cells in the 
ovary, in the lymphatic glands, and in the stomach. The cells are 
few in number, and are arranged in tubules and cylinders in the 
ovary. Are they to Ije regarded as secondary derivatives, or is the 
ovary the original focus? — the stomach, although showing by far the 
greatest amount of damage, being secondarily affected; or is there 
such a thing as cancerous diathesis due, say, to a contagium 
fluidum, and not to a corpuscular or morphotic virus ? 

Feh'uary 7th, 1899. 

20. A case of gastrectomy for carcinoma of the stomach. 
By Thomas F. Chavasse. 

THE patient, a man aged 64, was admitted into a medical ward of 
the General Hospital, Birmingham, on October 8tb, 1898, 
under the care of my colleague, Dr. Rickards. He complained of 
pain in the stomach, flatulence, and vomiting, and for a long time 
had suffered from dyspepsia, but there was no history of heema- 
temesis ; the bowels were generally constipated. 

On examination there was marked retraction of the abdominal 
walls, and extremely flaccid muscles. A swelling was visible 
below the left costal margin, and on palpation a large sausage- 
shaped tumour was evident in the epigastric, umbilical, and left 
hypochondriae regions. The tumour was of firm consistence, and 
moved freely with each respiration. On percussion there was an 
area of absolute dulness. On examining the stomach contents no 
free hydrochloric acid was found ; lactic acid was present at first, 
though absent at a later date. The patient had marked atheroma 
of the vessels, and also suffered from chronic bronchitis and 
emphysema. The urine contained no abnormal constituents. 

On November 2nd, after a consultation, the patient was removed 
'o :i surgical ward. 

Operaiion (November 3rd). — The abdomen was opened by a small 
incision to ascertain the extent of the growth and adhesions. The 
stomach being found much contracted and moveable, it was 
decided to make an attempt to remove it entire. The incision was 

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therefore enlai^ed and extended from the xiphoid cartilage to the 
umhilicus. Commencing at the left border of the greater omentum 
and working towards the pylorus, that membrane was divided sue- 
cessively between pressure forceps, and its vessels tied with silk 
ligatures. The same process was undertaken with the lesser 
omentum, from the pylorus to the lower end of the cesophagus. 
Two clamps were then applied l^eyond the pylorus, and the 
duodenum divided between them. The lower opening was closed 
with Lembert's sutures, and dropped into the peritoneal cavity. 

The organ having been separated from its adhesions, it was 
found that the carcinoma bad ulcerated through the stomach wall, 
and a round opening nearly the size of a sixpence was disclosed on 
the anterior surface near tlie cardiac end. The gastro-splenic 
omentum was next clamped and divided piecemeal. The oesophagus 
being pulled down as much as possible, a clamp was applied as high 
up as the diaphragm permitted, a second one being placed just above 
the cardiac end of the stomach, and, a division having been effected 
between them, the stomach was removed. By sponge packing the 
large cavity was kept quite dry, and some enlarged mesenteric glands 
were dissected out. An attempt was then made to fix a Murphy's 
button in the oesophagus so as to connect it with the jejunum, but 
partly owing to the retraction of the oesophagus and to the move- 
ments of the diaphragm, and partly to the extreme friability of 
the oesophageal walls, after several ineffectual attempts this pro- 
ceeding had to be abandoned. No effort was made to unite the 
bowel and gullet by suture, as the aneesthetist gave warning that the 
operation should soon be concluded. Accordingly the lower end of 
the oesophagus was closed by silk sutures and left in situ. The 
divided end of the duodenum was stitched to the lower end of 
the abdominal wall, the remainder of the wound being closed in 
the usual manner with silkworm-gut sutures. The duration of the 
operation was one hour and fifty minutes. 

After removal to bed there was a little restlessness, and three 
hours after the operation a quarter of a grain of morphia was given 
subcutaneously. The patient slept during the afternoon, and was 
fed with nutrient enemata given four-hourly. 

At 6 p.m. the temperature was 97**, pulso 96 ; the patient com- 
plained of thirst, flatulence, and a desire to vomit. During the 
night he slept for six hours. 

November 4th. — At 11.30 a.m. the duodenum was opened, a 

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catheter introduced, and the patient fed with peptonised milk, egg, 
and brandy. Diiodenal feeding was carried on four-hourly. The 
temperature remained subnormal. The heart's action becoming 
weaker strychnia was administered subcutaneously. 

The patient died of cardiac failure on the morning of the 5th, 
forty hours after the completion of the operation. 

At the post-mortem examination made on November 6th the 
main points noted are — 

Body much emaciated. 

Heart, — Small and contracted. Marked atheroma of the walls 
of all the larger arteries examined. 

Lungs, — Some old pleuritic adhesions. Hypostatic congestion 
at both bases. 

(Esophagus.— hength. 8 J inches, lower i inch, soft, friable, and 
infiltrated with new growth. Lower end completely occluded and 

Fig. 15. 

Carcinomatous stomach removed during life. 

Abdomen. — There was no general peritonitis. The cavity where 
the stomach had rested was dry and entirely shut off by adhesions ; 

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the duodenum was securely fixed to the lower end of the abdominal 

Stomach. — Small and very much contracted, bent on itself, and 
measuring 9\ inches along its greater curvature and 3J inches 
along the lesser. The organ was almost entirely solid and its cavity 
nearly completely obliterated, its lumen avei*aging i to f inch ; 
its weight was 6 ounces. A perforation, the size of a sixpence, 
existed anteriorly near the cardiac end. Numerous glands show- 
ing secondary growths were found along the smaller curvature. 

For the microscopical sections and the description of the same 
I am indebted to Dr. McDonald, pathologist to the Gkneral 
Hospital, who reports that there is hypertrophy of all the coats of 
the stomach wall, but especially of the submucosa. Although the 
new growth was apparently diffused throughout the organ, the 
sections near the pylorus show only fibrous thickening of the sub- 
mucous coat, without any evident cancer cells. Examination of 
the enlarged glands along the lesser curvature showed typical 
spheroidal-celled secondary growths. Proceeding towards the 
cardiac end, there was increasing infiltration of the submucous coat 
with irregular spheroidal cancer cells, this being the prevailing 
type of new growth throughout. In places, however, the cells were 
armnged as in an ordinary scirrhous cancer, and at one point 
there was a nodule coming up to the surface of the mucous mem- 
brane, in which the cell clusters had a distinct peripheral layer of 
columnar cells. In the mucous membrane, and in some places in 
the other coats of the stomach, there is a wide-spread small-celled 
infiltration, with marked congestion and some small haemorrhages > 
this is well seen near the special nodule previously referred to, and 
in the same neighbourhood there is a distinct fibrinous exudation 
on the surface of the mucous membrane showing leucocytes and 
degenerating desquamated cells. It would appear, therefore, that 
an acute inflammatory condition was superadded to the cancer, but 
there is no evidence that, this was in any way connected with the 
perforation which existed, and which was apparently due to can- 
cerous ulceration. No organisms were detected in any part of the 
stomach wall. 

The chief points of interest are the mixed form of carcinoma 
present, the existence of ulceration and perforation together with 
the diffuse induration and extreme contraction of the organ, and 
the apparently superadded inflammatory process. 

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The method emplojed for removal of the stomach was, iu the 
main, that successfully carried out by Dr. Carl Schlatter, of Zurich, 
the exception being the effort made to join the oesophagus and the 
jejunum by means of a Mai*phy's button instead of by sutures. 
The patient being very feeble, it was conjectured that a saving of 
time might be thus effected. The difficulties met with were the 
short portion of the oesophagus left, the depth of the wound, and 
the movements of the diaphragm hampering one's manipulations. 
The oesophageal wall, owing to its invasion by the neoplasm, 
proved very friable, and any tension upon the encircling ligature 
resulted in a tearing out. The button was three times placed in 
position, each time with more difficulty, before the attempt was 

The examination of the oesophagus after death showed that its 
walls were infiltrated to a point three quarters of an inch higher 
than the point of removal. 

Unless the operation for removal of the entire stomach is em- 
ployed instead of pylorectomy, the cases in which it can be 
employed with chance of a successful issue must be very limited. 
If the cardiac end of the organ be the site of the commencement 
of the new growth, then, as in this case, the walls of the oesopha- 
gus will probably be implicated to an unknown extent. Fixation 
to and implication of the neighbouiing organs will also prove de- 
terrents. In the present instance, excepting the lower end of the 
oesophagus, the whole of the ditieased tissue proved to have been 
removed. April ISth, 1899. 

21. Carcinoma developing in the cicatrix of a gastric ulcer, 
[Card specimen.) 

By H. R. Belcher Hickman, MB. (introduced by Dr. Lazarus- 

TPhe specimen was taken from the body of a woman aged 29, who 
-L died in St. George's Hospital. The patient was a general 
servant; she had never been strong, but gave no history of any 
definite illness. She had suffered for three months preceding her 
death from epigastric pains, vomiting, and general dyspeptic sym- 

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ptoms. Oq admission she complained of pain and swelling of the 
abdomen. A hard swelling eould be felt occupying an area about 
the lower edge of the liver. The patient gradually got worse, and 
died three weeks after admission. 

At the autopsy the lungs were found to be cedematous, and there 
were numerous small nodules of new growth on the pleura and in 
the lung substance. There were also nodules infiltrating the 
mesentery. The liver contained several masses of growth. The 
pancreas was involved in a growth about the pylorus. 

The specimen showed a dilated stomach, the mucous membrane 
of which appeared normal about the fundus, but towards the 
pyloric end of the lesser curvature there was a slight rough cicatrix 
of a former gastric ulcer, 1^ inches in diameter. Still nearer the 
pylorus was a slightly raised mass, which, with a cicatricial fibrosis, 
had caused a stenosis of the pylorus barely admitting the little 
finger. There was also great hypertrophy of the sphincter 

Microscopically the primary growth was found to be a spheroidal- 
celled carcinoma composed of various-sized cells; the secondary 
deposits were made up mostly of rather large spheroidal cells. 

Hemmeter and Ames (* Medical Record,' September 11th, 1897) 
describe a similar case (but in this there was also phlegmonous 
gastritis), and give a full biography of cases published to that date. 
Hayem met with a case in which the ulcer was entirely latent 
during life (*La Presse mcdicale,' August 4tb, 1897). Dieulafoy 
describes a case in which the ulceration was very extensive, and 
the growth was composed of vaiiously sized cells ('La Presse medi- 
cale,' November 10th, 1897). The subject is briefly mentioned by 
Debove and Remond (* Traits des Maladies de TEstomac ') ; they 
credit Dittrich {* Prager Vierteljahresscbrift,' v, 1884, p. 1) with 
being the first to record a case of cancer as a complication of gastric 
ulcer, and they give also the following references : 

j:i*«»/oAr.— * Deutsche Wochenschrift,' 1243, 1890. 
Biack.—' Wien. med. Presse,* No. 13, 1890. 
Werner."* WiiTtt, incd. Correap.,' Nos. 22—24, 1869. 
Lebert.—* Die Krankheiten des Magens,* Tiibingen, 1875. 
Flatour. — Inaug. Dissert., Munich, 1887. 

Haeberlin says that in 3 per cent, of cases of cancer of the 
stomach the previous existence of ulcer is certain ; whilst he is of 
opinion that in 4*2 per cent, it is nearly certain, and in 3 per 

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cent. vei7 probable. Hauser, in a ftiemoir on the subject (Leipzig, 
1883), asserts that 5 to 6 per cent, of pyloric caucer has started in 
chronic ulcer. Descriptions of similar cases are to be found in the 
* Pathological Transactions,' vol. ix, p. 200 ; vol. xl, 1890 ; vol. xlvi> 
1895. February 7th, 1899. 

22. A specimen of duodenal ulcer from a case ofrneliena neo* 
natorum, {Card specimen.) 

By T. D. Lister, M.D. 

A SPIRIT preparation consisting of the stomach, liver, and the 
duodenum as far as just beyond the biliary papilla. The 
duodenum has been opened and laid out on the under surface of 
the liver. The stomach has been opened and closed again by 
sutui;es along its greater curvature, and is turned over so as to 
show the opening of the pylorus into the duodenum, and is there- 
fore not closed right up to the valve. The head of the pancreas 
and the bile-ducts remain attached under the duodenum, and the 
gall-bladder is intact, containing very dark green bile. 

A shallow ulcer is seen near the cut edge of the duodenum, a 
quarter of an inch from the pylorus. Its edge is slightly raised, 
and shelves gradually to the centre of the ulcer and into the sur- 
rounding bowel. At the centre the ulcer deepens suddenly into 
the submucous tissue, and its base is semi-transparent for an area, 
of about 2 mm. by 1 mm. 

Li the recent condition the ulcer was plugged by a small clot 
which remained adherent for some time, but which was eventually 
loosened, and is shown in a small vial beside the specimen. This 
clot apparently extended into a rather large vessel in the base of 
the ulcer, which seemed to be derived from the gastro-duodenal 
artery. The pylorus was closed, and there was no blood in the 
stomach. The intestines were, however, full of blood, red and fluid 
in the small intestine, but darker and more or less coagulated in 
the colon and rectum. There was no other change in the whole of 
the intestinal canal, and the raucous membrane appeared quite 
normal on being washed. 

Abstract of case. — Baby C — , aged 3 days, was admitted to the 

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East London Hospital for Children, under Dr. Donkin, on the 29th 
of November, 1897, having begun to pass blood in large quantities 
on the 28th per rectum. There was no heemorrhage from any 
other mucous surface. 

On admission the temperature was 97°, and the patient was con- 
tinually passing blood per rectum, A saline enema was adminis- 
tered, and was followed by very abundant haemorrhage, leaving 
the patient very anaemic and collapsed, and the patient died on 
the 80th, when four days old. The skin was thought to be icteric 
the day before death, and a few small petechial spots appeared on 
the right cheek and side of the neck on the same day. 

At the autopsy the condition already described was found. The 
funis was still adherent, but dried brown and shrivelled. There 
was no oedema or congestion, either superficial or deep, in the 
tissues in the neighbourhood of the umbilicus. The mucous mem- 
branes were generally anaemic, as were also the solid viscera. 
There were no petechiae on the serous membranes. In the lungs 
were a few scattered, small, superficial, pyramidal infarcts of a deep 
brilliant ciimson colour. Their bases on the suiface of the lung 
were usually of a square shape, and the largest was about a quarter 
of an inch square at its base, and extended about three eighths of 
an inch into the lung. These infarcts were not attended by 
pleurisy, nor were they appreciably raised above the surface. They 
were very shai*ply defined from the surrounding anaemic lung 
tissue. There were no infarcts in any other organs. 

Comment, — In this case the probable cause of all the lesions 
would seem to be the separation of thrombi from the umbilical 
vein, which could be swept at once into both the general circula- 
tion and into the lungs — the view expressed by Landau in 1874. 


Rilliet and Barthez,—* Traite dcs Malad. de TEnfance,' 2nd edit. (20 cases), 
vol. xi, pp. 295—310. 

Silbermann,—' Gerhardt's Handb.,' iv (37 cases), S. 415. 

Landau. — " Ueber Melaena der Neugeborenen," * Habilitationsscbrift,' Breslan, 

OWo«?*K.— 'Med. mod.,* August 25tb, 1897. 

Neumann,^" Melaena Neonatorum," * Arcb. f . Kinderb.,' xii, 1891. 

Homen.— Art, in * Cent, f . allg. Putb.,' il, 1892. 

Kundrat and Jr*ncitei.— Quoted in * Starr's Text-book,' i, p. 93. 

May 16M, 1899. 

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23. Healed perforation of duodenum after passage of gall-stones. 
{Card specimen,) 

By Cecil F. Beadles. 

DUODENUM with its surrounding attachments, the bowel being 
laid open along its upper surface. 

There is a small cicatricial depression seen on the inner lining of 
the duodenum just short of an inch from the pylorus, which is 
quite distinct from the orifice of the biliary pancreatic duct, the 
latter being situated SJ inches from the pyloric opening. This 
depression corresponds to the firm adhesion of the wall of the gall- 
bladder on the outside, where also folds of the omentum have 
become drawn in during the process of cicatricial contraction, and 
in this thickened tissue a small biliary calculus lies embedded. 

The gall-bladder was shrunken and tightly contracted over a 
single faceted calculus, in size that of a marble, and weighing 
20 grains. Its surfaces are somewhat worn, showing that al- 
though other calculi were at one time present, they had not 
recently left the viscus. No fluid existed, and no other stones 
were found. 

The old adhesions above referred to, and a certain amount of 
matting of the intestines in the neighbourhood, clearly prove a 
localised peritonitis had been set up at the time stones had left the 
gall-bladder, these having possibly passed both into the bowel 
and into the peritoneal cavity. 

The liver was small, and weighed but 29 i oz. ; the larger bile- 
ducts were dilated. 

Prom a woman aged 70, who died insane after a short residence 
in Colney Hatch Asylum. It appears that she had been paralysed 
for eleven years. She had lived in the West Indies for five years 
some forty years ago, and had ague while there. Had drunk 
lieavily of late. Her father died insane. No history was obtained 
that pointed to gall-stone disease or peritonitis. She was admitted 
in a very feeble and paralysed state, and died demented v^itbin six 

At the autopsy advanced cardiac and arterial disease was found, 


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and the brain presented appearances common to senile dementia^ 
but no lesion was discovered to account for the old paralysis. 

January I7tk, 1899. 

24. Thj'ee cases of sprue. 
By J. H. Deysdale, M.D. 

CASE 1. — Man aged 49 years, admitted to St. Bartholomew's 
Hospital under the care of Dr. Church on February 10th, 

History. — In February, 1897, he went on the hospital ship to 
Benin ; while there he suffered from fever and ague. 

In March of the same year he returned to England, and then 
went to Crete. While there he had ague again, and began to 
suffer from diarrhoea. Five or six dirty white stools in the twenty- 
four hours passed without pain. His mouth began to be " sore,'* 
and he had " ulcers " on the tongue. 

In May he went to China, and suffered all the voyage from 
diarrhoea and wasting. The diarrhoea has never ceased. No 
history of dysentery. Has lost over 7 stone in weight during his 
illness. While in the hospital the stools were always coloured. 
Temperature never raised. He died on April 6th, 1898. 

Postmortem examination. — Very emaciated. Tongue smooth, 
papilloB hardly visible. (Esophagus natural. 

Stomach. — Small and tubular, resembling in shape the colon rather 
than a healthy stomach. Near the fundus and the pylorus the 
walls of the stomach were much thinned and quite smooth. The 
body was thickened, apparently from muscular hypertrophy and 
contraction, the mucous membrane being thrown into folds. In 
this region the circumference of the stomach when laid open only 
measured Si inches. 

Small intestine. — Jejunum natural. Ileum: hypersemic zones 
alternated with zones where the valvulse were absent. In the 
latter situations the gut was very thin, and print could easily be 
read through it. No obvious ulceration. 

Large intestine. — A single follicular ulcer. 

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Liver (45 oz.). — The gall-bladder contained oraoge-colonred bile, 
and the bile-duct was patent. 

Pancreas- — Bather small, but not harder than natural. 

Lunge. — Miliary tubercle of both lungs and pleursB. 

A bacteriological examination of the stools only revealed the 
B, colt communis. Unaltered bile was found on examination in the 

A blood examination showed only ausBmia of the usual secondary 

Microscopical examination. — Ton.gue. — In the portion cut the epi- 
thelium was everywhere thinned, and in places altogether absent. 
The underlying tissue appeared healthy. 

stomach. — ^Portions of the thinned areas near the cardiac and 
pyloric orifices showed an atrophic condition of all the structures 
composing the wall. The superficial portion of the mucous mem- 
brane stained badly and appeared almost structureless. This was 
probably in part due to post-m^ortem digestive action. In the 
deeper portion there was some increase of connective tissue in 
between the gland tubules. The cells lining the tubules are 
deformed and small, and at the cardiac end it is impossible to dis- 
tinguish between the central and parietal cells. 

In the body of the organ corresponding to the ** hypertrophied *' 
portion the mucosa appeared less changed, the increase in thickness 
being due to a greatly thickened submucosa, a great increase of the 
fibrous tissue in that region having taken place. 

Small intestine. — The wall was very thin, and all the structures 
composing it seemed to be atrophied. In places the villi have 
quite disappeared, and where they remain have lost their epitheliiun 
and are converted into shrunken tags infiltrated with small round 
cells. Many of the cells lining the crypts of Lieberkuhn are 
deformed, and the lumiua of the crvpts themselves in places have 
become dilated. The fibrous tissue in the submucosa is relatively 
if not absolutely increased. 

The pancreas shows no marked change, the connective tissue not 
being increased in amount. 

Gasb 2. — A woman admitted to St. Bartholomew's Hospital 
under the charge of Dr. Church on May 16th, 1898. 

History. — ^Eighteen months before admission, while in Bombay, 
the patient began to suffer from diarrhoea and sore tongue. The 

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stools were white and copious. Formerly weighed 15 stone; 
shortly before death reduced to 6^ stone. No history of dysentery. 
After admission the diarrhoea continued until the patient died. 
The stools were usually faintly coloured, but were sometimes quite 
white or grey. The individual stools were not copious, but were 
often frothy and offensive. 

Pad-mortem examination, — Very emaciated. 

Tangne quite smooth and shrivelled. 

CEsophagiM natural. 

Stomach natural. 

Small intestine. — Much thinned. No active ulceration. In the 
lower 4 feet of the ileum at intervals there are scars left by 
the healing of ulcers. They are pigmented and puckered, and%re 
situated opposite the attachment of the mesentery. 

Liver (28 ounces). — The gall-bladder contained bile ; bile-duct 
patent. There was some bile in the duodenum. 

Pancreas small and firm. 

Spleen looks natural ; weight 7 ounces. 

A bacteriological examinaiion of the stools gave a negative result. 

A blood examination showed a well-marked anaemia of a secondary 

Microscopical examination. — The tongue was not examined, 
having been preserved intact as a museum specimen. (Esophagus 
and stomach natural. 

Small intestine. — The changes resemble those in the first case. 
The villi are much diminished in size, have lost their epithelium, 
the whole of the remaining structure ^being infiltrated, though not 
densely, with small round cells. 

Pancreas, — Sections of the organ show a most extraordinary 
change. The connective tissue throughout is much increased in 
amount. Strands of fibrous tissue, visible in stained specimens 
to the naked eye, give the specimens at first sight almost the 
appearance of a coarse hepatic cirrhosis. All trace of alveolar 
structure is lost, the cells being tightly packed within the inter- 
lacing strands of new-formed fibrous tissue. The cells themselves 
are many of them degenerate and vacuolated, both the nuclei and 
cell protoplasm staining badly. 

Case 3. — A man admitted to St. Bartholomew's Hospital under 
the care of Di. Brunton on April 22nd, 1898. While in India in 

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November, 1896, began to suffer from diarrhoea. The stools were 
white and frothy, but contained no blood, and were passed without 
pain. In 1894 had an attack of dysentery. 

After admission the patient passed stools greyish white in colour, 
frothy, copious, and foul- smelling. Sometimes the stools were 
yellowish, and occasionally on standing turned green from the 
presence of biliverdin. 

A blood examination shortly after admission showed a second ar^r 
anaemia of a mild grade. Before death the aneemia became more 
pronounced, without altering its character. 

A bacteriological examination of the stools gave negative results. 

Poat-mortem examination, — Much emaciated. 

Tongue. — Papillae over dorsum dwarfed. Surface quite smooth, 
no loss of substance. 

(Esophagus natural. 

Stomach smooth and thinned over the greater part. 

Sm^all intestine. — Thinner than normal, but not quite trans- 

Colon, — The ascending and transverse portions of the colon were 
somewhat contracted, and the walls apparently much thickened. 
The mucous surface is covered by what looks like a greyish- white 
granular exudation. 

The descending colon contains several large ulcers, irregular in 
shape, with well-defined, rather sharply-cut edges. 

Pancreas natural. 

OaU'hladder contains orange-coloured bile. 

Microscopical examination. — Tongue. — In parts, though quite 
smooth, the surface epithelium, so far from being thinned, is con- 
siderably increased in thickness, but as in the other case (1) the 
underlying structures seem unchanged. 

The small intestine. — ^The changes were similar to those present 
in the other two cases, though the atrophy of the mucous mem- 
brane was more pronounced. 

The ascending and transverse colon. — The thickening evident 
macroscopically proved to be due entirely to an enormous increase 
of the connective tissue in the submucosa, the mucosa and the 
muscular coats being thinner than natural. The surface of the 
mucous membrane in places was fused into a solid mass of inflam- 
matory exudation, all the normal structure being lost. The exuda- 
tion consisted of a structureless mass, containing in its substance 

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a few small round cells. The homogeneous substance did not give 
the staining reactions o£ fibrin. Towards the deeper portion 
remains of glandular structure could be seen. The cells were 
cubical and the lumina of the crypts dilated, giving them a cystic 

Pcmereas natural. 

Bemarks, — In none of the cases was the disease in an active 
state, so that one can hardly describe the changes as those of 
sprue. The changes are, however, those commonly found in 
patients who die from the effects of sprue, and include not only 
the alterations due to the local effects of the disease, but also 
changes in the portions of the bowel uuaffected by the primary 
disease, due to what is practically a death from starvation. 

The bacteriological examination showed in all cases an over- 
whelming predominance of the B, coli communis. The result is 
only what might be expected when the period in the disease at 
which the examination was undertaken is considered. 

In all the cases the normal colouring pigment of fceces was 
present. In Case 1 the stools were always coloured, but in 2 and 3 
the examination was made when the stools were greyish white in 
colour. At this time there was no difficulty in extracting, by means 
of acidified alcohol, a large quantity of deep brown pigment. 
Whether the colounng matter is present as a colourless chromogen, 
or whether the excess of fat which is present in these stools masks 
the colour which is present, I have not been able to decide. 

AprU ISth, 1899. 

25. Fatal summer diarrhcea with acute enteritis. 
By F. W. Andebwbs, M.D. 

THE specimens shown are from a case of fatal summer diarrhcea, 
which is of some interest not only because the intestinal lesion 
found post mortem was unusually intense, but because the bacterio- 
logical examination afforded a probable explanation of what was 

The patient was an unmarried girl of 19, in previous good health. 
In August last she was attacked by diarrhoea and vomiting, slight 

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at first, but soon becoming more intense, till on the erening of the 
second daj she was admitted to St. Bartholomew's Hospital in a 
state of profound collapse, from which she never rallied. Death 
occurred some fif ty-six hours from the first onset. There is little 
to relate of, the symptoms. The case was apparently an ordinary 
one of so-called "English cholera." While under observation 
the stools were frequently passed, colourless, and not unlike the 
rice-water evacuations of Asiatic cholera, from which, indeed, 
apart from bacteriological examination, the case could not be dis- 
tinguished. At the jpost-mortemy held twenty-four hours after death, 
the sole lesion found was an enteritis of unusually intense cha- 
racter. The mucous membrane of the entire jejunum and ileum 
was of a vivid crimson colour and somewhat thickened. No ulcera- 
tion was found, but the solitary follicles stood out very con- 
spicuously, and were evidently swollen. Peyer's patches were not 
so much affected. The specimen shown has been prepared with 
formalin, and gives a good idea of the condition, though its colour 
has faded considerably. 

It will be admitted that so intense an enteritis is rarely found in 
fatal acute diarrhoea. I have seen many post-mortems on similar 
cases, and I cannot remember to have seen anything approaching 
it. Commonly, in my experience, there is little or no evidence of 
enteritis after death, even in the most acute and rapidly fatal 
cases. At the most one sees a little injection of the intestinal 
mucous membrane, with or without slight swelling of the lymphatic 
structures. Even these may be absent. Within a few days of the 
occurrence of the present case we had at St. Bartholomew's another 
post-mortem on an adult man who died of acute diarrhcea, as 
sudden, as rapid in its course as the preceding, and not to be dis- 
tinguished from it in clinical features. Yet the intestine showed 
no sign whatever of any inflammatory change ; indeed, no sign of 
the cause of death was to be found post mortem. 

There must clearly be reasons for such differences. The causa* 
tion of summer diarrhoea is still an unsettled question, though it is 
generally conceded to be of microbic origin. Personally I accept 
the Bacillus enteritidis sporogenes (of Klein) as the probable cause 
of the disease. Not only is it constantly present in a virulent form 
in fatal summer diai*rhoea, but what is known of its life history 
fits in very well with the hypothesis framed by Ballard in explana- 
tion of the epidemic incidence of the disease* It is, however, out- 

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side my aim to discuss the matter here, as the point I wish to 
suggest is that over and above the iufectiou, whatever it be, which 
caused the primary diarrhoea in this case, there was also a definite 
streptococcus infection of the bowel, which seems to me possibly to 
account for the special character of the lesion. 

Both a stool passed before death and a portion of the contents 
of the ileum taken at the autopsy were subjected to bacteriological 
examination. The spirillum of Asiatic cholera was searched for 
in the usual routine manner, and was not found. The BaciUtis 
erUeritidis sporogenes was found readily enough in both specimens. 
It was demonstrable microscopically by Gram's method of stain- 
ing, though not in very large numbers, and it was obtained in pure 
culture in the ordinary way by inoculating milk tubes with the 
fsBcal material, heating these to 80° C. for ten minutes, and then 
incubating anaerobically in Buchner tubes. Of the whey from one 
such tube, forty-eight hours old, one c.c. was injected subcu- 
taneously into a guinea-pig and proved highly virulent, causing 
intense local oedema and gangrene, with death in about thirty-two 
hours. All this is what may be found in almost any case of acute 
summer diarrhoea. The special feature of this case lay in the very 
large number of streptococci present in the intestinal contents; 
they formed, indeed, the great bulk of the organisms present, 
which in my experience is unusual. (A stained specimen of the 
stool was shown.) Sections of the inflamed intestine stained by 
ordinary bacterial dyes showed enormous numbers of short bacilli 
(presumably B. coli cowwnwww, Proteus, &c.). Sections stained by 
Gram's method showed in the necrotic mucosa small numbers of 
streptococci and B. enteritidis sporogenes, not merely on the sur- 
face, but actually in the tissue. Ordinary agar-agar cultures made 
from the mucous membrane yielded a large crop of B. coli communie 
and other organisms, but amongst these were a number of strepto- 
coccus colonies, and the organism was obtained in pure culture. 
I am not prepared to state that it was identical with Streptococctts 
pyogenes ; it made broth uniformly turbid, and formed compara- 
tively short chains. I regret that I did not test its virulence. 

These observations, imperfect as they are, seem to me to indicate 
that the special characters of the enteritis in the case described 
were due to streptococcus infection. I am, however, far from 
asserting that such infection was the primary cause of the disease, 
for I imagine that it is only infrequently to be found in fatal 

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sammer diarrhoea. I conceive it to have been a secondary infec- 
tion grafted upon an ordinary summer diarrhoea. The occuiTence 
of streptococci in enteritis is well known ; amongst others, Hirsch 
and Liebmann have described the condition (* Centralbl. f. Bakt. 
u. Pamsitenkunde/ Bd. xxii, pp. 369 and 376), and more recently 
Escherich. October 18th, 1898. 

26. Two uTvumal cases of intussusception. 
By D'Abcy Power. 

IBBiNG forward this evening two specimens of intussuscepted 
bowel to show that death may result from the two opposite 
conditions of absolute irreducibility, and from an intussusception 
which is too easily reducible. Both cases were in the hospital at 
the same time, and it was my misfortune to operate upon them on 
successive evenings. 

A. R—, a girl aged 5 months, was admitted to the Victoria Hos- 
pital for Children, 16th June, 1898. A cooling powder had been 
administered to her on the 13th inst., and had caused a single 
action of the bowels. The child was suddenly seized with a scream- 
ing fit on the evening of the 14th inst., and it was evident that she 
was in great pain. She began to vomit at once, and on the follow- 
ing day she passed blood and slime. The vomiting and discharge 
of blood-stained mucus continued until her admission on the 16th. 
The child had always been healthy before this attack, and had 
never suflPered from diarrhoea. 

There was no distension of the belly at the time of the patient's 
admission to the hospital, but there was some tenderness on palpa- 
tion, especially upon the right side. No tumour could be felt 
through the abdominal walls, but by rectal examination it was 
easy to detect a swelling situated about 3 inches from the anus, and 
the finger was stained with blood when it was withdrawn. 

The child was ansosthetised, and as soon as the abdominal walls 
were relaxed a distinct sausage- shaped tumour could be felt in the 

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left flank. An attempt was made to reduce the iatussusception by 
irrigation with hot saline solution for five minutes, under a pres- 
sure of three feet. As no alteration took place in the size or 
position of the tumour the abdomen was opened immediatelj 
by a 3-inch incision. The intussusception was exposed and an 
endeavour was made to reduce it in the ordinary way. It proved 
to be quite irreducible, and I therefore stitched part of the small 
intestine to the abdominal wall, selecting a piece of the ileum as 
near as possible to the tumour. The patient was collapsed and 
feeble after the operation, but she survived until the next day. 

A post-mortem examination showed a large ileo-caecal intussus- 
ception. The intestines above the invagination were not greatly 
congested, and a piece of ileum about 2 inches from the begin- 
ning of the intussusception had been opened and attached to the 
abdominal wall. There was no trace of peritonitis. 

The intussusception was cut out without previous reduction. It 
was hardened, and a longitudinal section was then made through 
it. Fig. 16 shows that it was of au extremely complex nature. 
The primary invagination was ileo-csecal, of the ordinary descend- 
ing type, the apex of the invagination consisting of the congested 
and thickened ileo-csecal valve, with the openings of the ileum and 
vermiform appendix. The primary invagination was enveloped in 
a second intussusception passing in the reverse direction, that is 
to say, of the retrograde variety, and this retrograde intussuscep- 
tion was itself complicated by a third intussusception, also of the 
retrograde kind. The primary intussusception and the firet retro- 
grade invagination had occurred during life, for their apposed 
surfaces were glued together with inflammatory exudation. The 
third invagination, which was much smaller, was formed after 
death by a wrinkling of the bowel. The primary intussusception 
measured 3^ inches in length, the retrograde invagination was 2^ 
inches long. The section showed that two lymphatic glands were 
carried down in the first intussusception, and that both were in- 
flamed. The ileum measured 11 mm. in transverse diameter, and 
the colon was 19 mm. across. 

This specimen was extremely complicated, but it is an important 
one, for I believe it to be an example of a form of intussusception 
which is by no means uncommon. It is a particularly deadly 
variety, — first, because distension of the colon has no effect in 
relieving it; and secondly, because after a laparotomy any attempt 

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Fio. 16. 


A semi-diagrammatic drawing of a longitudinal section tbroagh a descending 
ileo-c»cal intussasception (a), complicated b^ a retrograde or ascending in- 
vagination (d). The puckering at o and o'was more marked when the 
specimen was fresh, and gave the appearance of an additional intussuscep- 
tion, d is the thickened ileo-cfecal valve, e is the vermiform appendix. 

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to reduce the intussusception tends to increase the retrograde inva- 
gination and so make matters worse. It was impossible to reduce 
the intussusception in this particular case, because the youth of the 
child and the amount of bowel involved prevented the tumour 
being brought to the surface, and it had to be manipulated, there- 
fore, as it lay in the small abdominal cavity. 

The original drawing of this specimen is in the museum of St. 
Bartholomew's Hospital, No. 457a. 

The second specimen is as simple as the former was complex. 
The patient was a boy aged 6 months, who was admitted to the 
Victoria Hospital for Children on June 16th, 1898, under the 
care of my colleague. Dr. Walter Carr, with the history that he had 
fainted on the 14th inst. The attack of syncope was followed by 
vomiting, and on the following day ho passed blood and slime but 
no fsBcal matter. The blood-stained mucus was passed four times 
on the day before his admission to the hospital, and he suffered 
much pain. The vomiting continued at intervals from the first 
attack until the time he was seen. 

The patient had been suckled for the first three months of his 
life, and after he had been weaned he was fed upon cow's milk and 
barley water. Two months before he had suffered from congestion 
of the lungs and inflammation of the bowels. 

On admission to the hospital he appeared to be a healthy and 
well-nourished child, presenting no physical signs of disease. No 
abdominal swelling could be felt either on palpation or jper rectum. 
He had one motion on the evening of his admission, passing a 
little blood with it, and he was sick after his food. It is reported 
on the following day, the 17th inst., that he had been sick through 
the night, and that his aspect was bad, but no swelling could be 
felt in his abdomen. 

He got worse during the day, and at 8.30 p.m. I was called in to 
treat the case as one of intussusception. The patient was anoBs- 
thetised, and it was easy to feel a sausage- shaped tumour in the 
upper part of the abdomen. An unsuccessful attempt was made 
to reduce the intussusception by irrigation with hot salt solution 
under a pressure of three feet, and the abdomen was then opened 
immediately by an incision carried just to the right of the middle 
line. I introduced my fingers, and as soon as I had lightly grasped 
the bowel just below the tumour the intussusception reduced itself 
spontaneously. I satisfied myself that the ileo-colic angle was fully 

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tmravelled and then closed the abdomen. The operation was not 
attended with any satisfactory result, for there was no action of the 
bowels ; the temperature rose to 103°, and the child died twenty- 
four honrs after the operation. 

The post-mortem examination showed the presence of an ordinary 
ileo-csBcal invagination, which was quite easily reducible, for there 
were no adherent surfaces. 

A month or two after the cases which I have just recorded came 
under my observation, Mr. Lucy, of Plymouth, sent me the accom- 
panying specimen to show before this Society, saying, " This is the 
description of a case I saw in consultation eight days ago. A 
delicate girl, thirteen years of age, was seized with violent pains in 
the right iliac region four days before I saw her, and vomiting fol- 
lowed by almost complete obstruction of the bowels, but there was 
no passage of blood or mucus nor any tenesmus. When I saw her 
the abdomen was uniformly distended, especially tympanitic in the 
epigastrium, but dull in either flank, a sign which gave way to reson- 
ance on rolling her over. There was no visible peristalsis, the rectum 
was empty and ballooned, and the child indicated a spot to the left 
and just above the level of the umbilicus as being most tender. 

" I thought there was a band or volvulus, and advised imme- 
diate operation. The abdomen was opened just below the 
umbilicus, and in the middle line. Clear fluid escaped, and a 
coil of distended small intestine was drawn down and secured by 
a few points of suture to the transversalis fascia and parietal 
peritoneum. The wound was then packed round with gauze, and 
the intestine was opened, allowing large quantities of green fluid 
and gas to escape, with evident relief to the heart and respiration. 
It proved, however, to be one of those " too late " cases we see so 
often, and she died poisoned in six hours. 

"I obtained a posUmoriem examination, and found that the 
enterostomy had been made three feet from the pylorus, and one 
foot on the proximal side of the obstruction. I removed the 
distended coil entire for further examination, noting that beyond 
it there were four feet of deeply congested ileum ending at the 
ileo-C8Bcal valve. A subsequent examination of the intestine 
showed that the gut narrowed suddenly a foot below the arti- 
ficial anus and disappeared beneath a horseshoe-shaped coil ot 
purple and distended intestine. This coil of intestine contained 
an intussusception, and on slitting open the intussusception I 

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found about tliree feet of collapsed and slatj-blue ileum, packed 
away and adherent between the entering and returning layers. 
This portion of the ileum ended in the intussusception proper." 

It is clear, I think, from Mr. Lucy's description, that this is a 
very unusual form of enteric intussusception, similar in some 
respects to my first specimen. It is an intussusception enclosed 
in a sheath of bowel, but with the additional complication that a 
very considerable length of the small intestine has slipped in 
between the two layers of the intussusception itself. I have 
thought, therefore, that the case should be recorded in the Society's 
• Transactions,* for I know of nothing like it. 

January Srdy 1899, 

27. Appendix vemiiformis in which a pin was lodged. 
(Card specimen,) 

By H. A. Lediajbd, M.D. 

THE appendix was removed post mortem from the body of a 
man aged 23, who died of gangrene of the lung in the Gum- 
beriand Infirmary in February, 1899. 

The post-mortem was made by Dr. Wade, Assistant House 
Surgeon, who was not led to examine the appendix region by any 
symptoms, for during life thei-e were none. The discovery of the 
pin was purely accidental. For a distance of two and a quarter 
inches from the free extremity the appendix is thick and a little 
dilated, and at the junction of the healthy part of the appendix 
with the diseased portion there is an area of ulceration of the 
mucous membrane the size of a threepenny piece, due possibly to 
irritation from the sharp point of the pin. The pin lay with the 
head at the extreme tip of the appendix. The length of the pin is 
about one and a half inches. 

May IGth, 1899. 

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28. Peculiar condition of the colon in pernicious anaemia} 
By H. MoBLEY Fletcher, M,D. 

THESE specimens from a case of pernicious anaemia are sbowu on 
account of the unusual lesions present in the intestines. 

The case was a typical one of pernicious anaemia. The patient, 
a hair-cutter agf d 84, was admitted three times to St. Bartholo- 
mew's Hospital under Dr. Hensley's care for this complaint. I 
am indebted to Dr. Hensley for his kind permission to refer to the 
clinical notes. 

The first occasion on which the patient was admitted was in 
June, 1897, and he presented well-marked and typical signs of the 
disease. As so often occurs in these cases, great though temporary 
improvement took place. 

In June, 1897, the condition of his blood was — heemoglobin 17 
per cent. ; red corpuscles 920,000, white corpuscles 3000. 

In October, 1897, the haemoglobin Ijad risen to 73 per cent. ; red 
cells to 3,340,000, white 3000. 

In March, 1898, he was again admitted. His haemoglobin had 
fallen to 18 per cent. ; red corpuscles were 1,200,000, and white 
corpuscles 8000. There was some epistaxis and moderate pyrexia, 
the temperature being generally 100^ at night-time. 

He was readmitted in September, 1898, with aggravated sym- 
ptoms due apparently to an attack of pleurisy, with some conges* 
tion of the base of the right lung, and he died three days later. 
His temperature varied during these days from 108^ to 106^. 

Two days before his death his blood was examined. Haemo- 
globin was 19 per cent. ; red corpuscles 700,000, white 2000. The 
legs were oedematous. 

The day before his death he had small frequent stools, four per 
diem, which are stated in the notes to have been '* evidently the 
result of constipation ;" at no time did he have diarrhoea. 

The jpoet-mortem examination was made by Dr. Qurrod. The 
notes are as follows : 

A spare man ; well-marked rigor mortis ; no haemorrhages. 

Brain weighed 48 oz., and was natural. The spinal cord was 
not examined. 

1 St. Bartholomew's Hospital Museum, No. 1995b. 

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(Edema of both lurigs with slight pleurisy at the right base. 

The heart weighed 16 oz. It was hypertrophied. The valves 
were natural. There was well-marked ** tabby cat " striation of 
the muscular tissue, which gave no iron reaction. 

The stomach was natural. 

The liver weighed 87 oz., and exhibited a well-marked iron 

The galUhladder was full of dark brown bile. 

The spleen was large, weighing 15 oz. ; it gave no iron reaction. 

The kidneys weighed 8 oz. each, and gave a well-marked iron 

The pancreas, ahdominal lymphatics, and supra-rendls gave no 
iron reaction. 

The pectoral muscle gave no iron reaction. 

Bones, — The marrow of the clavicle was pale in colour and gave 
no iron reaction. That of the tibia was of a very deep red colour, 
and gave a vivid iron reaction. I am showing sections of the tibia 
both stained and unstained, though the unstained specimen has 
lost unfortunately some of the brightness of the red colour. 

The intestines. — Peyer's patches were very long, some of them at 
least four inches. The mucous membrane showed remarkable 
roughening in the colon and lower part of the ileum. It appeared 
as if covered with a warty growth of yellowish -brown colour. In 
places this appearance was continuous, in other parts patchy with 
intervals of healthy mucous membrane. The affected intestines 
were peculiarly tough, thick, and leathery. Nothing abnormal 
was noticed in the intestinal vessels. I am showing a portion of 
the colon, and sections are placed under the microscope. 

Further comment on the case or the post-mortem notes is un- 
necessary, except that it is interesting to note the fact that this 
case shows very well the way in which certain organs may exhibit 
the so-called iron reaction to a marked degree, while in others, 
notably the spleen, it is sometimes entirely absent. 

The microscopical changes in the intestine are as follows : — ^There 
is necrosis, in parts complete, of the mucous membrane occurring 
in patches, associated with great hypersBmia. In places hsBmor- 
rhages have occurred. The glandular structure can be made out, 
though greatly altered and covered by masses of necrotic material. 
These are evidently recent changes. The increased thickness of 
the gut is largely due to the fibrotic condition of the submucosa, 

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which is also hsBinorrhagic and CBdematous. The fibrosis can only 
be regarded as due to some older inflammatory affection of the 

This condition of the intestines in connection with pernicious 
anaemia appears to be very unusual, and I have been unable to 
find records of any similar case. The question naturally arises, is 
this condition simply coincidental, or is it in any way associated 
with the primary blood disease, as other lesions of the alimentary 
tract, especially of the stomach, have been considered to be ? 

The duration of the illness — eighteen months— is opposed to the 
view that this condition of the intestines could have existed for 
any great length of time without giving rise to some symptoms, 
such as diarrhoea, when we consider that the entire colon was 
affected. In the clinical history of the case there were present 
none of the alimentary disturbances which have been described by 
Hunter^ and others as occumng in pernicious anaemia. Vomiting 
and diarrhoea were conspicuously absent, while constipation was 

There is no doubt that in many cases of pernicious anaemia, 
gastritis with marked changes in the mucous membrane of the 
stomach is a prominent symptom, and that atrophy of the gastric 
glands may possibly be a cause of the disease as suggested by Dr. 
Samuel Fenwick.* It is far more probable, as Hunter has argued, 
that these lesions are not the cause but are only associated with 
the primary disease. 

The changes in the intestine which I am showing, appear to me 
to have been produced late in the course of the disease — perhaps 
quite near its termination. How have they been brought about t 
No cause of irritation of the mucous membrane can be found; 
arsenic was given over long periods, though never in larger doses 
than 5 minims of Fowler's solution. The normal appearance of 
the stomach and duodenum would exclude the possibility that this 
drug might have produced the lesion. Purgatives were occasion- 
ally given, but never calomel. 

The microscopical appearance of the intestine almost suggests 
thrombosis of the mesenteric veins by the great congestion of the 
mucosa and oedema of the submucosa, but there was no evidence 

1 • Lancet,' Sept. and Oct., 1888. 
« Ibid., 1887, vol. ii, pp. 1, 89, 77. 

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of this at the jjosUmoriem, and the intestine would have been dark 
red in colour rather than a pale yellow. 

Eepeated hsBmorrliages into the submucosa might perhaps 
account for some of the changes, but the hsemorrbages which are 
apparent under the microscope are too minute and limited to have 
produced a result so extensive, and there is no evidence of pig- 
mentation pointing to former hsemorrhage. 

The only other hypothesis I can bring forward, but for which 
there is no evidence, is that the extensive changes in the intes- 
tines may have been caused by some neurotrophic lesion. Cases 
have been described by Banti, Eichhorst, and others in which 
definite lesions in the alimentary canal have occurred apparently 
as the result of changes in the sympathetic system whether of 
the ganglia or the plexuses of Auerbach and Meissner. In such 
cases the nerve changes are probably due to degeneration resulting 
from impaired nutrition. It is conceivable that something ana- 
logous may have occurred in this case, but there is no evidence 
for it. 

As I have already pointed out, the intestinal lesions are of two 
kinds : the one, an old inflammatory change affecting the sub- 
mucosa and resulting in fibrosis and thickening ; the other, and 
more recent, a coagulation-necrosis of the mucosa. These changes 
may possibly be accidental, but it is far more probable that the 
older change in the submucosa is an intestinal lesion comparable 
to those described in other parts of the alimentary canal by 
Hunter and others, and which may be directly associated with the 
blood disease. The necrotic condition of the mucosa is probably 
accidental and connected with the acute termination of the 
disease. Lecemher 20th, 1898. 

29. A specimen of diffuse ulcerative colitis with secondary 
acute interstitial hepatitis. {Card specimen,) 

By T. D. LisTBE, M.D. 

AFOBMALiN preparation, consisting of the last four inches of the 
ileum, the ileo-ccecal valve, the ccecum, and all the large 
intestine. The intestine is laid open, and the whole of the mucous 

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membrane of the vermiform appendix and of the colon is seen to 
be covered with minute ulcers. There is no ulceration in the four 
inches of ileum exhibited, though there is a moderate degree of 
hyper»mia. The ulcers of the colon are mostly hemispherical 
depressions of 1 to 2 mm. diameter, but in many places they have 
run together, forming small oval or even irregular ulcers with 
deeper and steeper edges than have the single ulcers. In a few 
instances, chiefiy in the sacculi between the longitudinal bands, 
the ulcers have a fissured linear form, but there are none of any 
form greater than 5 mm. in length. Their distribution is quite 
irregular, and bears no particular relation to the follicles, many 
follicles being normal and many ulcerated, and many of the ulcers 
being placed between the follicles. The process is most marked in 
the ascending colon, the vermiform appendix, and in the sigmoid 
flexure. There is also a greater degree of congestion in these parts 
than elsewhere, though the whole is congested. In the rectum the 
process is almost entirely follicular. There is nowhere any 
** flaking " or membranous sloughing. 

In the recent st-ate the colon contained both fresh and altered 
blood and some mucus, and in the rectum there was some bile- 
stained feculent mucus, but no other liquid or solid feeces any- 
where in the intestines. 

Cass. — The case was that of a boy aged 5, admitted under the 
care of Mr. H. B. Eobinson at the East London Hospital for 
Children on April 11th this year, with somewhat anomalous 
symptoms of intussusception, for which abdominal exploration was 
performed. The clinical history of the case is dealt with else- 
where by Mr. H. B. Eobinson, to whom I am indebted for permis- 
sion to show the specimen. The symptoms were not relieved, and 
the boy died eight days after the operation with gradually in- 
creasing haemorrhage from the bowel, and finally hsBmatemesis, the 
wound having healed perfectly. 

At the autopsy the large intestine was found in the condition 
described above. The abdominal wound was completely healed 
deeply and superficially. There was general diffuse broncho- 
pneumonia. The internal organs were all strikingly anaemic, 
except the mucous membrane of the small and large intestines 
and that of the stomach. The mucous membrane of the stomach 
and small intestine was acutely and very generally congested, but 
nowhere presented any ulceration. There was altered blood in 

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the stomach, and fresh and altered blood all through the intes- 
tinal tract, which seemed to be derived from no definite focus or 
foci, but to arise from a more or less general oozing. 

The microscopical preparations shown include sections of the 
colon and of the liver. The latter organ in the recent state was of 
a very pale colour and somewhat fattj. It was rather firm. 

Sections of the colon show, firstly, an extensive destruction of 
the glandular epithelium, the columnar epithelium being entirely 
absent in many of the tubes, and in most of them being only 
represented by a few loose cells lying irregularly in the lumen, 
these cells having separated in masses of one to ten or twelve. 
Secondly, a small-celled infiltration of the basement membrane 
and connective tissue, especially close to or at the fundus of the 
tubes. Thirdly, an extension of this infiltration into the sub- 
mucosa from some of the tubes, which is traceable in some 
instances as an infiltration beginning in the connective tissue 
between the glands, extending more deeply to the fundus, and 
then into the submucosa to expand into a considerable mass 
of round cells. Fourthly, by an extension of this process, the 
formation of ulcers in which the glandular tissue is entirely lost. 
Fifthly, the dilatation of the vessels of the mucosa and submucosa 
into quite considerable blood spaces. In many places the in- 
flammatory change can be traced by the masses of round cells into 
the muscularis mucosse. 

Sections of the liver show, firstly, a severe diffuse cellular infiltra- 
tion ; where a lobule has been cut through centrally there is 
seen to be a zone of round cells completely surrounding it, and 
this process is general throughout the perilobular and interlobular 
tissue ; there seem to be no foci ; the cellular infiltration extends 
to a greater or less extent towards the centre of the lobule, but in no 
instance can there be found any aggregation of cells in or near the 
centre of a lobule ; the average thickness of the inflammatory zone 
is about one quarter of the radius of the lobule. Secondly, a large 
proportion of the liver cells contain fat globules, especially those 
of the intermediate zone, the cells otherwise appearing normal. 
Thirdly, the bile-ducts are normal. Fourthly, the tissue is very 
anaemic. In sections of the liver stained for organisms, numerous 
rods can be seen, but their nature was not ascertained by cultures, 
and the autopsy was made more than twenty-four hours after 

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Somewhat similar cases of colitis leading to clinical difficulties 
are described. 

(a) By Dr. Samuel Adams, in Starr's ' Text-book/ vol. i, 488. 
(h) By Rosenheim, in Eulenberg's * Encyklop. Jabrb.,' iv, 1894. 
(c) By Ashbjf and Wright, * Diseases of Cbildren/ p. 87. 

May 16th, 1899. 

30. Villous papilloma of rectum. {Card specimen,) 
By T. Cabwabdine, M.S. 

THE apecimen was a portion of a ?illous tumour dischai^ed 
spontaneously per anum. It must lia?e been at least the 
size of a closed fist, judging from the quantity of villous material 
which came away. The patient was a youDg woman about 25, 
who for the last four years had suffered agonies from piles and 
prolapsus ani, and latterly bits of jelly-like material had frequently 
come away, appearing like villous fronds on examination. 

The piles were treated by operation, but for special reasons no 
further search per rectum was desirable at the time. A week after 
the operation the patient passed a very large quantity of what 
the nurse called ** mucus," and for the twelve months subsequently 
the patient has been perfectly well, with no indications of papilloma 

The villous fronds were in some cases three inches long, branched, 
and often with somewhat clubbed terminals. The substance was 
little firmer than that of a jelly-fish, rendering it quite impossible 
to suspend the fronds in a bottle owing to friability. There was 
no indication of a much thickened base, and no suggestion of 
malignancy. The spontaneous discharge of a villous papilloma is 
a rare but recognised event. January 17 th, 1899. 

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31. Enterolith from the rectum, {Card specimen,) 
By SAMUEL G. Shattock. 

AN irregularly oval concretion about 2 inches in chief diameter, 
which was removed (in 1857) from the rectum of a lady 
69 years of age ; its weight immediately after removal was 3 oz. 
(avoirdupois). A concretion had previously been removed by Dr. 
Oldham, of Guy's Hospital. The central cavity was filled with a 
crumbling material mixed with shining crystals, some of which 
remain projecting from its sides ; the material was fusible, and 
may be assumed, therefore, to have consisted of phjosphate of lime 
mixed with ammonio-magnesian phosphate. The peripheral part 
of the calculus, which has a coarae radial structure, is composed 
largely of organic matter with ammonio-magnesian phosphate and 
a small proportion of phosphate of lime. The specimen was pre- 
sented to the museum of the Eoyal College of Surgeons last year 
by Mr. Norris F. Davey. 

As 1 was anxious to ascertain whether the periphery contained 
any calcium oxalate, a portion was kindly examined by Mr. Gordon 
Salamon, but with a negative result. Intestinal calculi of this 
substance occur amongst herbivora, where they may attain con- 
siderable dimensions ; and although none such have as yet been 
recorded in the human subject, it is not unlikely that the progress 
of vegetarianism may bring about their formation, seeing that the 
substance in question is derived solely from that ingested in vege- 
table food. May 2nd, 1899. 

32. Achroo-amyloid liver, spleen, and kidneys. 
By W. J. Hadlby, M.D. 

CLINICAL HisTOBT.—A man aged 75, taken ill suddenly with 
violent pains in abdomen, followed by oedema of legs and 
then ascites, after thirty-five days getting gradually worse, was 

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admitted into hospital with enormous ascitic distension of abdomen, 
great oedema of flanks and legs, marked general wasting, and a drv, 
brown tongue. Janndice supervened a few days after admission. 
Several hundred ounces of fluid were drawn from the abdomen. 
The liver was felt to be much enlarged. The urine was very scanty 
(only 10 — 19 oz. in twenty-four hours), contained bile and a 
considerable quantity of albumen (one tenth to two thirds). 

There was never any rise of temperature; vomiting came on, 
and the man gradually sank twelve days after admission and 
forty-seven days after the onset of the disease. 

Post-mortem appearances. — The lower limbs and scrotum were 
osdematous, and there was marked jaundice. There was a little bile- 
stained fluid in left pleural cavity, and the lungs were OBdematous. 

The heart was contracted, cavities practically empty. There was 
acute endocarditis (small granulations) of the mitral valve. 

Abdomen, — Much excess of fluid, adhesion round liver and spleen. 

Spleen (12^ oz.) very hard, no reaction to iodine (like "ague 


Kidneys (15 oz.) peel readily, surface smooth. Cortex slightly 
increased, a few cysts, no haemorrhages. A few isolated points 
stain dark brown with iodine. 

Liver much enlarged, hard; no reaction to iodine, though it pre- 
sents typical bacony appearance of lardaceous disease, but feels 
harder. Tbere was perihepatitis, and several coils of intestine 
were matted together and adherent to liver and spleen. 

Microscopic appearances, — Liver, — With ordinary staining, an in- 
filtration is seen between and in the cells, chiefly affecting the central 
zone of the lobule, but being for the most part widely spread through- 
out the organ. This material is stinictureless and homogeneous, 
seems to replace the whole liver cell, and, although having the 
general appearances and anatomical distribution of lardaceous 
degeneration, it does not give the characteristic staining reactions 
of that material on the one hand, nor, on the other, does it give 
those of hyaline degeneration. This material, therefore, which is 
somewhere in position between amyloid and hyaline (both deriva- 
tives of flbrin), has been styled achroo-amyloid, on account of its 
non-staining properties. Dr. Bullock, to whom 1 am greatly in- 
debted for his aid in working out this case, has tried a whole 
pharmacopoeia of reagents with hardly any success in staining it. 
These attempts have been made on fresh material and also on tissue 

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hardened in sublimate and alcohol. Briefly it does not give any of 
the staining reactions of amyloid , nor any of those of hyaline. Ana- 
tomically it is amyloid ; chromatically it is neither amyloid nor 
hyaline. It stains faintly with orcin, eosin, logwood, and methyl 

Spleen. — Here too, as in the liver, there are the typical histo- 
logical appearances of diffuse amyloid disease, but no charactenstic 

Kidneys,— These are the only organs that show any characteristic 
amyloid staining ; for in a few of the Malpighian tufts an imperfect 
or hybrid reaction to methyl and gentian violet is seen. Otherwise 
the kidneys show the appearances of chronic nephritis contracting, 
but still large. 

Staining methods. 

Spleen and liver. — 1. Against true amyloid, — Iodine, iodine and 
H2SO4, thionin, iodine green, and polychrome methylene blue ; no 
amyloid reaction. Methyl and gentian violet : evanescent, impos- 
sible to ^x colour. 

2. Against true hyaline. — Van Gieson's stain (picnc acid and 
Saurefuchsin) : indefinite colour, yellowish brown. 

3. Weigert's fibrin method. — No reaction. 

K^idw6y«.— Some Malpighian tufts give hybrid reaction to methyl 
and gentian violet. 

April \^th, 1899. 

33. Acute degeneration of liver cells supervening in the course 
of chronic cirrhosis. {Card specimen.) 

By F. Pabkbs Webbb, M.D. 

THE liver of a man aged 20, working as a tailor in London, who 
died with cerebral symptoms and jaundice, following an 
attack of vomiting and diarrhoea. When I saw him the day before 
his death he was unconscious, but sometimes moved restlessly or 
cried out when disturbed. He had previously been wandering in 
his mind and noisy. The pupils were equal, of medium size, and 
did not react to light. The corneal reflex was present. The tongue 

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was dry and brown. Eespirations shallow, about fourteen in the 
minute. Pulse 120, regular, soft. Temperature 97° F. No 
abnormal physical signs were found in the thorax or abdomen. 
The urine was slightly acid, clear, and of a dark brown colour, 
changing to green on the addition of nitric acid ; there was no 
precipitate on boiling, but acetic acid either before or after boiling 
gave rise to slight opacity ; no sugar. 

Past history. — Quite uncertain. 

Necropsy. — The hrain presented nothing abnormal. 

The heart was of about normal weight, and showed nothing note- 

In the lungs a few small subserous petechial patches and one 
small recent haemorrhage infarction was observed. The bronchial 
glands were slightly enlarged. 

Kidneys rather hard, capsule slightly adherent in parts. 

Spleen weighed about 7\ oz. 

Pancreas apparently natural. 

In the large intestine some redness of the mucous membrane 
and enlargement of the lymph-follicles were observed. 

The liver (weight about 55 oz.) was of rather firm consistence, 
as it would be if there were some fine cirrhotic process in progress. 
No hobnail appearance. Microscopic examination shows, firstly, 
that there is a considerable amount of uniform cirrhotic change, 
mainly " interlobular " in distribution ; and secondly, that the liver 
cells have undergone a very marked (doubtless acute) fatty 

Remarks. — Owing to the deficient history the explanation of 
the case is not quite obvious. No information pointing to the 
exact cause of the cirrhosis was obtained, and no bacteriological 
examination of the liver was made. The pathological anatomical 
sequence of events seems to me clearer. A chronic interlobular 
fibrosis (whatever its cause may have been) of the liver doubtless 
already existed, when the acute degeneration of the gland-cells gave 
rise to the fatal termination with jaundice and cerebral symptoms. 

It is almost useless to speculate as to the original cause of the 
hepatic disease. For such a chronic interlobular cirrhotic change 
without much increase in the bulk of the whole organ there are 
probably many possible causes. Aufrecht's experiments, however, 
throw much light on the whole subject. This observer ^ produced 
1 'Deutflcbes Archiv fiir kliu. Medicin,' Bd. Iviii, S. 802. 

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a cirrhosis of the liver in rabbits by small repeated doses of phos- 
phorus. He thinks that small doses of phosphorus lead to 
partial atrophy of the hepatic cells in the outer zones of the acini, 
giving rise to the appearance of interstitial inflammation between 
the acini. Some of the cases of acute atrophy supervening on 
chronic cirrhosis of the liver in man may be explained by supposing 
that the chronic action of some irritant leads at first to a pro- 
gressive cirrhosis, and that afterwards a sudden increase of the 
irritant process (such as may be set up by intestinal catarrh) 
brings on acute degeneration of the remaining glandular cells and 
the symptoms of icterus gravis. February 7th, 1899. 

34. Diffuse mfiltration of the liver in congenital syphilis. 
By H. MoRLEY Fletcher, M.D. 

THE specimens ^ were taken from the body of a female child aged 7 
weeks, who was under my care in the Children's Hospital, 

She was three weeks old when admitted. The mother stated that 
ten days after birth she noticed that the child's belly was swollen 
and apparently tender. There had been no jaundice or vomiting. 
The bowels were regular, the stools green, but not offensive. The 
child was said to have had snuffles, but no rash. There were seven 
other children alive and healthy, and besides these the mother had 
one bom dead, but no miscarriages. No further evidence of a 
history of syphihs was obtainable. 

The child appeared well nourished on admission, was free from 
any form of skin eruption, and had no snuffles. 

The abdomen was greatly distended, and the superficial veins 
were prominent. The liver occupied the greater part of the 
abdominal cavity, the edge reaching half an inch below the 
umbilicus. The spleen could not be felt. Slight peritoneal friction 
could be felt over the liver when the child cried There was no 
great abdominal tenderness and no evidence of free fluid in the 
abdomen. The case was treated as one of congenital syphilis with 
mercurial inunction, and later with grey powders. 

^ St. Bartholomew's Hospital Museum, No. 2202?. 

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When the child was five weeks old it began steadily to lose flesh, 
its general condition up to this time having been fairly good. The 
temperature throughout the course of the illness was irregular, 
ranging from 100° to 102°. There was also a good deal of 
diarrhoea, the stools being generally of a brown or yellow colour, 
though occasionally green. There was no trace of jaundice at any 
time, nor was there oedema. The child died when seven weeks old, 
having been in the hospital for four weeks. I am indebted to Dr. 
Shardlow, the resident medical officer, for these notes. 

The post-mortem examination was made by Dr. Shardlow. 

The body was wasted. Neither eruptions nor petechise were 

The lungs and bronchial glands were natural. 

The heart weighed 1 oz., and had a patent foramen ovale. 

Abdomen. — There was no ascites. 

The liver weighed 28 oz. It was generally enlarged and very 
hard. There was slight roughening on the upper surface, which 
probably caused the peritoneal friction felt during life. The cap- 
sule was thickened. The upper surface was fairly smooth, but had 
a blotchy appearance. The under surface was much more uneven 
and nodulated, though the irregularities could hardly be said to 
amount to scarring. 

The right supra-renal was firmly adherent to the under surface 
of the right lobe of the liver. The gall-bladder was distended 
with bile. Nothing abnormal could be detected in the portal or 
hepatic veins. There were no petechisB on the serous surfaces. 
The section of tlie liver showed a remarkable mottled appearance, 
due to large brown patches mingled with paler areas. The brown 
colour was due to haemorrhage. The amount of fibrosis was not 
apparent to the naked eye, though there was obviously but little 
normal liver substance left. No circumscribed masses or nodules 
resembling gummata could be seen. 

Both supra-renals were nearly as large as the kidneys, and on 
section had a transparent appearance with a deep chocolate colour, 
which was much darker in the medullary portion. The usual dis- 
tinction between cortex and medulla was entirely lost. 

The spleen (i oz.) showed no naked-eye changes. 

The kidneys appeared normal. 

The intestines and mesenteric glands were normal. 

Microscopical examination of the liver. — The capsule is thickened. 

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There is an extreme degree of fibrosis, which is most marked in the 
portal spaces. The fibrosis is so extensive, and has led to such great 
destruction of liver cells, that it is difficult to recognise any well- 
marked pericellular cirrhosis. Here and there may be seen a few 
small isolated clumps of fairly healthy-looking liver cells. There is 
a nearly continuous narrow layer of almost normal liver cells imme- 
diately under the capsule. In the dense masses of fibrous tissue 
can be seen very numerous slender branching tubules, some con- 
taining bile pigment. These somewhat resemble the so-called 
newly formed bile-ducts, but it is more probable that they are 
the remains of liver cells separated in colunms by the fibrous 
tissue, and much compressed. In places the continuity of these 
slender columns of cells with a clump of healthy cells can be 

The most striking microscopical change is a diffuse infiltration of 
the liver by small round cells. Under a high power it is found that 
the majority of these cells are small round cells, not unlike those 
found in some primary sarcomata of the liver. Between the cells 
can be made out a delicate reticulum and spindle-shaped cells with 
oval nuclei. There is evidently very active connective-tissue forma- 
tion in progress. There is great vascularity and considerable 
hsemorrhage in these parts. In no place is there the slightest 
trace of any caseation. The vessels show no change. The sections 
gave no lardacein reaction. 

Sections of the supra-renal capsules show an extensive destruc- 
tion of the cortex by a small-celled infiltration closely resembling 
that in the liver. The whole of the medullary portion is filled with 
heemorrhage and organising blood-clot. Haemorrhage into the 
supra-renals in infants is not an event of great rarity, but the 
cases described are generally associated with purpuric eruptions 
and fever. I have been unable to find any similar cases recorded 
in connection with congenital syphilis. In describing a case of peri- 
cellular cirrhosis in an infant of ten weeks, Penrose ^ states that the 
supra-renals were " of a dull red-grey colour, quite imlike ordinary 
supra-renal colour." No microscopical account is given. The 
colour is the same as in the case I am describing. There are 
hemorrhages in the kidney also, but the structure appears other- 
wise normal. Sections of the spleen show nothing of interest. 

The question naturally arises as to the nature of the extensive 
* Peurose, • Path. Soc. Tranf.,' vol. xxxix, 1888, p. 135. 

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small round-celled infiltration present in the liver. There are some 
points of resemblance between this and two cases of primary round- 
celled sarcoma of the liver which have been described in the * Trans- 
actions ' of this Society, one by Dr. Norman Dalton,^ and the other 
by G. Heaton.2 The former of these shows an infiltration of the 
organ by cells closely resembling those I have described, but there 
can be little doubt that this was a case of congenital sarcoma. In 
neither case was there anything approaching the amoimt of fibrosis 
which is found in congenital syphilis. 

It must be admitted that the evidence of syphUis in this case, 
though strong, is not conclusive, but the cirrhotic changes in the 
liver can hardly be due to any other cause. A series of closely 
similar cases, with diffuse infiltration of the liver, has been described 
by Marchand.'^ In most of these the liver was greatly enlarged, and 
of a dark brownish-red colour. Ascites and petechise were gene- 
rally present. Marchand points out that this diffuse infiltration is 
only found in children who die shortly after birth. It is possible, 
as Wilks ■* suggested in describing a case of syphilitic cirrhosis in an 
infant in 1866, that some such changes might be present in the active 
stage of acquired syphilis. Hutinel and Hudelo ^ describe the con- 
dition in the foetal or new-bom liver as a ** diffuse embryoual infil- 
tration," a term implying that an active proliferation in the young 
connective-tissue elements is set up by an exciting agent brought 
probably by the umbilical vein. Hence the resemblance to a 
sarcomatous growth, another form of connective-tissue prolifera- 
tion. It is possible to mistake a syphilitic liver with this diffuse 
infiltration, or " diffuse gummatosis," as Hutinel and Hudelo have 
called it, for a congenital diffuse round-celled sarcoma, and it is 
probable that some of the so-called diffuse sarcomata which have 
been thus described are really syphilitic in origin. 

November Ist, 1898. 

1 'Path. Soc. Trans.,* xxxvi, 1885, p. 247. 

« Ibid., xlix, 1898, p. 140. 

5 * Centralblatt fur allgem. Path.,' 1896, Bd. vii, S. 273. 

* S. Wilks, 'Path. Soc. Trans.,' xvii, 1866, p. 1G7. 

^ Hutinel and Hudelo, ' Archiv. de Med. exp^rimentale,' 1890, p. 509. 

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35. Diffuse syphilitic change in the liver. 
By F. Pabkks Weber, M.D. 

THE patient (a carman), C. W — , aged 47, was brought to the 
German Hospital, February, 1898, in an apoplectiform con- 
dition, due to cerebral heemorrhage. As evidence of syphilis (for 
which he had recently been under treatment) there was a perfora- 
tion of the palate and disease of both testes, one being uniformly 
enlarged and the other f ungating. The temperature varied between 
100-2° and 102*2° F. He lived three days after admission. The 
primary syphilis had probably been acquired several years ago. 

^ccrop«y. — Besides the cerebral hcBmorrhage and evidence of 
syphilitic disease of the testes, glottis, and palate, there was pneu- 
monia at the base of one lung, and slight interstitial fibrosis of the 

The spleen weighed about 14 oz., and microscopically presented 
nothing remarkable. 

The liver weighed ^7 oz., and was indurated, but no distinct 
gummatous masses or scarring were noted. Microscopic examina- 
tion of the organ shows a remarkable diffuse change, differing in 
degree in different parts. In the sections exhibited to-night the 
amount of change is very considerable; a great portion of the 
glandular cells have disappeared, their place being taken by a 
fibrous material, which in most parts is not very rich in nuclei 
The feature to which I wish to draw attention is that the fibrous 
change is generally most advanced in the central portions of the 
acini, and least noticeable around the portal spaces. In fact, the 
change is quite distinct from that. of all ordinary cases of cirrhosis, 
in that the best preserved liver cells are those at the periphery of 
the acini, precisely those which are most likely to be encroached 
upon in ordinary cirrhosis. 

This is not the only case in which I have observed the peculiar 
feature in question. Perhaps it is exclusively to be found accom- 
panying diffuse syphilitic change, and it is on this account that I 
have brought the present case before the Pathological Society. 

Professor Adami ^ has recently drawn special attention to the 

* ** On the Stages and Forms of Syphilis, with more especial reference to the 

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diffuse changes in the liver met with in some cases of acquired 
syphilis. He points out that the hepatic changes are found to be 
essentially of the same order, whether the affected liver be examined 
in the first year after primary syphilis or long afterwards, though 
the longer the time that has elapsed after infection the greater is 
the tendency to the development of cicatricial changes with contrac- 
tion and deformity of the organ. He writes : ** It is generally laid 
down that in tertiary syphilis affecting the liver, gummata, whether 
well-marked and caseous, or the cicatrised remains of such, with 
well-formed stellate surroundings of fibrous bands, are the charac- 
teristic changes in the organ, while a condition of generalised and 
pericellular cirrhosis is wanting. It must, however, be remembered 
that even years after the primary affection such cirrhotic change 
may be recognisable, and not a few cases are on record of such a 
condition." The diffuse change in the liver found in the present 
case abimdantly confirms Adami's words, though the precise lapse 
of time since the primary syphilitic infection is uncertain. Adami 
proceeds to describe special instances of tertiary syphilis of the 
liver in which he has met with circumscribed areas of pericellular 

A process of pericellular fibrosis must indeed be recognised as 
occurring in the liver of acquired syphilis, similar to that which 
has long been recognised as characteristic of hepatic disease due 
to congenital syphilis of children. Miliary gummata, moreover, 
certainly occur in the livers of adults as they do in those of infants, 
and in all probability in the acquired as well as in the congenital 
disease. In the present case, although the livpr showed no distinct 
gummata or scars from old gummata, there was a more or less 
generalised fibroid change, which may be regarded as the result of 
a process commencing with pericellular cirrhosis, analogous to that 
spoken of by Adami. 

A fact, however, which, as I have already stated, should be noted 
in the present case, is the decided tendency of the fibrotic process to 
invade the whole inner area of the acini, and to leave the outer 
zone of hepatic cells least affected. This tendency of the diffuse 
syphilitic change to spare the hepatic glandular cells nearest to 
the interlobular spaces is certainly not peculiar to the present case. 
I have noticed it in some other cases, though apparently it has not 
Hepatic Manifestations of the Disease," published in the 'Montreal Medical 
Journal,' June, 1898 ; and in ' Treatment,' London, November 24tb, 1898. 

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been recorded by other observers, wbo have perhaps regarded it as 
too unimportant to mention. There is, however, possibly a special 
significance to be attached to it, which I shall now endeavour to 

The glandular cells which in these cases suffer most are, I repeat, 
those of the middle and inner zones of the hepatic acini, those which 
are least affected in ordinary forms of cirrhosis, but which suffer 
most in chronic passive congestion (nutmeg liver*) and amyloid 
disease.^ The middle and inner zones of the acini are those sup- 
plied by the finest branches of the hepatic artery. In fact, this 
form of "diffuse syphilitic cirrhosis" may be termed "pericapil- 
lary " quite as justly as " pericellular." 

The distribution of the fibrotic change in ordinary cirrhosis, 
which is chiefly " periportal" (the glandular cells of the outer zones 
suffering especially), has been supposed by many to point to the 
portal vessels as the channels by which, in such cases, the agents 
are introduced which injure the hepatic cells and determine the 
fibrosis. The distribution of the change in a "diffuse syphilitic 
cirrhosis " (when it resembles that of the present case) has led me 
to suspect that some abnormal condition of the arterial blood-? 
supply may be the chief determining cause of this variety of 
cirrhosis. A striking histological feature in some cases of cardio- 
sclerosis (fibroid disease of the heart muscle) is that the most 
affected portions of the myocardium, where the muscle-fibres have 
almost completely undergone fibroid degeneration, are precisely 
those portions which are furthest removed from the small branches 
of the coronary arteries from which their blood-supply is derived. 
The cardiac change has, therefore, been supposed by some observers 
to be due to ischflemia brought about by an arterio-sclerotic change, 
which causes narrowing of the lumina of the small arterioles. In 
the case of the liver, however, the explanation of the somewhat 
analogous change which is shown by my sections must remain, at 
least for the present, still more doubtful. March 21«^, 1899. 

^ The change in the centres of the acini resalting from chronic pa«ftive con- 
gestion of the liver occasionally resemhles a real fibrosb when examined under 
the microscope ; the term " centro-acinous " cirrhosis has, I believe, probably 
incorrectly, been applied to it. 

> It may be remarked that sections stained with methyl violet for amyloid 
disease gave a negative result in the present case. 

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36. A case of cirrhosis of liver, apparently due to congenital 
syphilis, with thrombosis of the hepatic veins. 

By T. Chxjrton, M.D. 

A MAN aged 26, whose father died at fifty of apoplexy, his mother 
at fifty-six of ansemia, his elder and only sister in infancy, 
and who had never been strong, noticed some enlargement in the 
epigastric region two years ago ; but though somewhat sallow, and 
for the last three or four months rather languid and inefficient at 
his work, had not been seriously ill until a week before his death. 
On July 26th a planing machine weighing 6 cwt. fell upon, or 
rather, perhaps, against his right arm (? and side), bruising the 
arm severely. He could not work, but did not seem ill. 

On August 4th he had diarrhoea for two days. 

6th. — Abdomen began to increase in size. 

9th. — Felt weak ; abdomen larger ; occasional pain in it ; no 
superficial veins visible (Dr. J. H. Woods). Was walking about. 

10th. — Much more ascites ; surface veins conspicuous ; was sent 
the same evening to the Leeds Infirmary. The history of previously 
perfect health then given, but subsequently foimd to be incorrect^ 
caused a suspicion of hydatid. Tapping the lower abdomen 
obtained only 2 or 3 pints of blood-tinged fluid; after this a 
fluid thrill could be obtained over the liver in any position of the 
patient. On August 13th, as the man was worse, a small explora- 
tory incision was made over the liver margin. This showed the 
nature of the case, and that fluid had apparently been imprisoned 
between the liver and diaphragm. The fluid re-accumulated 
rapidly ; no peritonitis occurred, but the exhaustion increased and 
the patient died two days later. 

Necropsy, ^In the centre of the cirrhotic liver was found a 
hepatic vein containing an old whitish clot ; the other branches of 
the vein contained dark red fresh or recent clot. The mouth of the 
vein in the vena cava was very narrow and completely blocked by 
whitish clot, so that it was not easily found. Microscopically, the 
thrombi are in some parts adherent to or rather fused with the 
wall of the vein and the connective tissue beyond, as though the 
connective tissue had invaded the vein and projected into it. The 
main veins are not much, if at all, enlarged. The intra-lobular 


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radicles are, however, some of them distended. The portal veins 
are not thrombosed. The cirrhosis is diffuse, intercellular and 
chiefly monolobular. The outer parts of some of the lobules 
appear to have been converted into ** new bile ducts." The transi- 
tion is (or appears to me to be) traceable by the staining of the 
protoplasm of the liver-cells, which shrink until the bare nuclei — 
larger, rounder, and less deeply tinted than the connective tissue 
nuclei — form parallel rows Or small circles of nuclei lying in a canal 
formed by connective "protoplasm" or "basement membrane." 
No effusions of blood are visible. 

Upon the disputed question as to whether congenital syphilis 
can cause a fibrosis so uniform as this, and a phlebitis with con- 
sequent thrombosis, I can offer no opinion, but I have twice in 
the same patient treated a case of acute uniform enlargement of 
the liver in a yoimg man, four years after acquired syphilis, with 
mercury with suggestively rapid success. In the present case no 
other cause, lead, malaria, alcohol, dyspepsia and auto-intoxication, 
or acquired syphilis could be foimd. 

November let, 1898. 

37. Thrombosis of hepatic vein associated with cirrhosis of 
the liver, probably syphilitic. 

By W. S. Lazabus-Baelow, M.D. 

THIS specimen was obtained from the body of a boy aged 13 years, 
who had enjoyed good health until the last four months of 
his life. The commencement of his illness showed itself by 
enlargement of the abdomen, and he sought admission to hospital 
by reason of general languor and breathlessness, coupled with 
heematemesis and melsena. On admission the abdomen was 
noticed to be covered by a plexus of distended veins ; he was thin, 
slightly jaundiced, bore distended venules on the cheeks, and had 
considerable ascites with great respiratory distress. The edge of 
the liver was felt three fingers* breadths below the costal margin. 
With regard to the question of syphilis, the evidence available was 
(1st) that the mother had had no miscarriages up to this, the third 
child, but four afterwards ; (2nd) the histological character of the 

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hepatic fibrosis. The patient's teeth were normal, and he had no 
interstitial keratitis. There was no alcoholic history. During his 
sojourn in the hospital the patient was tapped twice, considerably 
over twelve pints of fluid being removed in the two tappings. He 
gradually sank after the second paracentesis. 

At the autopsy there was found a localised suppurative peri- 
tonitis. The liver weighed 2 lb., 10 oz., was granular and mottled on 
the surface. On the upper surface posteriorly was a large mass of 
cicatricial tissue which extended It inches into the depth of the 
organ and involved the hepatic vein. Numerous branches of the 
hepatic vein, both large and small, were occluded by partially 
adherent and decolourised thrombus. The cicatricial mass sug- 
gested a former gummatous condition, and its edges shaded off in 
the form of trabecules of fibrous tissue into the (macroscopically) 
normal substance of the liver. At the same time the branches of 
the portal vein served as centres of a fibrous-tissue overgrowth 
throughout the organ, so that a section revealed macroscopically a 
mottled surface, in which foci of what appeared to be normal liver 
substance were separated by irregular trabeculse of fibrous tissue 
which stretched in all directions. Here and there were seen 
sections of the occluded hepatic vein. 

Microscopically the liver, even in its apparently most nearly 
normal regions, showed the existence of a mixed fibrosis. The 
greater part was of the multilobular variety, but there was much 
of the intercellular type. None of the white masses in the liver 
were found to be gummatous. 

Remarks. — Thrombosis of the hepatic vein appears to be a some- 
what uncommon condition, nevertheless several cases are on record. 
In a communication by Kelynack* on the same subject, reference 
is made to a case published by Frerichs, and in the notes of & case 
reported by Gee^ reference is made to an autopsy made by von 
Becklinghausen, and published by Bosenblatt, in which the same 
condition obtained. In none of these cases was the occurrence 
of syphilis certain, though for the most part its occurrence was 
highly probable. In Gee's case, which was one of a child aged 
17 months, the hepatic veins were cut off from the inferior vena 
cava by a thin membrane, and the positions at which these veins 
should normally open into the vena cava were only represented 
^ * Medical Prets and Circular,' vol. cxv, 1897. 
« See 'St. Bart.'8 Hosp. Rep.,' 1871, p. 144. 

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by small dimples. In Kelynack's case the aperture of only one 
hepatic vein into the vena cava was distinguishable, and this was 
only large enough to admit a small probe. In the present case 
no abnormality of this kind was present. It is therefore 
impossible to determine how far stenosis induced by contraction 
of cicatricial tissue may play a part in inducing the thrombosis, 
but it must be mentioned that in Gee*s case it is expressly 
mentioned that the appearances about the jimction of the vena 
cava and the hepatic veins were quite dissimilar from those of 
ordinary scars. 

The specimen is preserved in the museum of St. George's 
Hospital, series ix, 174 I. November Ist, 1898. 

38. Liver in hepatic and portal thrombosis, {Card specimen.) 

THE liver weighed 46 oz., and to the naked eye appeared atrophied 
and nutmeggy. The portal spaces were unduly prominent, but 
there was no evidence of ordinary cirrhosis. 

Microscopically the liver cells are extremely atrophied and are 
shrunken, while the fibrous tissue of the portal canals is so pro- 
minent, that it seems difficult to doubt that it has undergone some 
increase in size. No doubt the atrophy of the liver cells shows up 
the normal fibrous framework, but some increased growth on the 
part of the interstitial supporting framework — a fibrous replace- 
ment — may well be expected under such circumstances. There is, 
however, no small-cell growth or evidence of recent hyperplasia in 
the fibrous tissue. 

The result of hepatic and portal thrombosis in this specimen, 
then, is atrophy of the hepatic cells and greater prominence of the 
fibrous framework. 

At the post-mortem there was an old parietal clot in the inferior 
vena cava, which did not interfere with the passage of blood 
through it. The adherent clot was situated near the openings of 
the hepatic veins. The right hepatic vein was blocked up by a 
thrombus of about the same age as that on the inferior vena cava, 

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wliile the left hepatic vein was free. There was no continuity 
between the thrombus in the right iiepatic vein and the parietal 
clot in the inferior cava, but it seems highly probable that they 
were not independent of each other. There was thrombosis of 
more recent date in the poiiial and splenic veins. It seemed not 
unlikely that the portal thrombosis was secondary to the throm- 
bosis in the right hepatic vein, and was related to venous stagna- 
tion and changes in the vitality of the liver cells. The spleen 
weighed 9 oz., and did not contain any infarcts; the weight is, 
perhaps, worthy of note as bearing out the general rule that in 
mere mechanical congestion, without any toxic or septic condition, 
the spleen is not enlarged. I have on several occasions, however, seen 
such enlargement in cases of simple thrombosis of the splenic vein so 
as to suggest that when the obstruction is so close to the spleen as 
in the efferent vein, the general rule which applies to the backward 
pressure, due to obstructive heart or lung disease, does not neces- 
sarily hold good. 

Death was due to concealed hflemorrhage into the stomach and 
intestines, which were found full of blood. There were numerous 
small hflBmorrhages into the skin, mediastina, and substance of the 
pericardium. These were probably due to hepatic insufficiency, 
allowing poisons which should have been destroyed to circulate 
freely. During life ascites which required paracentesis and rapidly 
reaccumulated occurred, and was evidently due to portal thrombosis. 

November Ihth, 1898. 

39. Cysts in the liver containing living Paramoecia coli. 
By A. E. EussKLL, M.D., and E. F. Buzzabd, M.B. 

THE patient was a man aged 69, who was admitted into St. 
Thomas's Hospital with carcinoma of the stomach. There 
was nothing imusual in the history nor in the course of the disease. 
Death occurred rather unexpectedly on May 6th, 1898. 

At the post-mortem examination there was a large malignant 
growth of the pylorus, the orifice being so stenosed as only to admit 

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the tip of the little finger. At the pylorus the growth was three 
quarters of an inch in thickness; it extended for four inches on 
the stomach, involving its circumference uniformly. The mucous 
membrane at the pylorus and for about two inches on the stomach- 
wall had disappeared. The stomach was enormously dilated. There 
were no secondary growths anywhere. The liver was normal, save 
for the presence of about a dozen small cysts situated in the region 
of the larger portal canals. In size they were barely as large as 
peas. They were firm to the touch, and contained brownish or 
orange-stained material of caseous consistence. The contents of 
two of the cysts were found to contain living Paramceda coli, which 
were identified by Dr. Hawkins. 

Examination of mounted and stained specimens showed that the 
cysts possessed a thick fibrous wall and almost structureless con- 
tents, the presence of what appeared to be faint nuclei suggesting 
indefinitely necrosed liver tissue. Unf ortimately the specimens did 
not show the parasites, presumably on accoimt of their delicate 
structure and poor staining qualities. 

According to Leuckart, the ParanKBcium eoli is an almost con- 
stant parasite in the pig, occurring in the csBCum and colon. It 
was first discovered as a human parasite by Leuwenhoek. 
Malmsten, however, was the first to recognise it as being asso- 
ciated with any pathological process, finding it in cases of diar- 
rhoea. Mitter regards it as proved that infection is conveyed in 
some means from the pig, either by inhalation of the encysted 
parasite, which may frequently be f oimd in the faeces of the pig, or 
through contaminated food. Schneidemuhl ^ gives references to the 
cases in the literature, altogether some thirty-six having been re- 
corded. The parasite appears to be associated with diarrhoeic con- 
ditions, and may be the exciting cause of an attack, or aggravate 
the condition in such diseases as cholera, dysentery, &c. In the 
case under notice, constipation with light-coloured stools appears to 
have obtained, and there was no history of any diarrhoea. 

As regards the cysts, the most reasonable assumption seemed to 
be that they owed their origin to an irritative process set up by 
these parasites, and that the latter found their way into the liver 
from the intestinal tract by way of the common bile-duct, the 

1 * Die Protosoen als Krankheitserreger des Menschen und der Hausthiere,' 

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bile-Stained contents of the cysts suggesting an origin in the bile- 
duct system. All the cysts were of about the same size, and it is 
possible that the parasites reached the liver simultaneously. 

At the meeting Mr. Shattock observed that the case was imique, 
and agreed as to the location of the parasites in the bile-ducts. 
The condition was in some respects comparable with that of 
psorospermosis in the rabbit's liver, in which the protozoa certainly 
wandered from the intestine up the bile-ducts; in fact, the con- 
dition was a " paramoeciosis." In the psorospermial liver the 
dilated ducts became the seats of complex papillary ingrowths, but 
nothing of this kind was shown in the cysts described. 

April ISth, 1899. 

40. Biliary calculi in children. 
By Gboegb F. Still, M.D. 

GALL-STONES are a rare occurrence in childhood, but it is important 
that it should be realised that this period of life is by no means 
exempt from them. The following three cases have occurred within 
the past six months at the Hospital for Sick Children, Great 
Ormond Street. 

Case 1. — Carrie B — , aged 9 months, was admitted imder the 
care of Dr. Lees for vomiting and wasting. The bowels were very 
costive; the child was irritable, and had been feverish at times; 
there was some cough. Feeding had been by breast for the first 
six weeks, then cow's milk (boiled) with barley-water, and lately 
condensed milk, to which more recently some brandy had been 
added. There was no history of jaundice. 

On admission the child was pale and emaciated; eyes sunken; 
f ontanelle depressed ; purpuric patches on the trunk ; no jaimdice. 
The heart and lungs were normal. The stools were hard and ** clay 
coloured." Purpura increased; vomiting was frequent but not 
persistent; diarrhoea supervened, and the child became more 
exhausted and died. No symptoms of colic or abdominal pain and 
no jaundice were observed during the five and a half weeks that 
the child was in the hospital. 

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Post-mortem. — Some broncho-pneumonia and recent pleurisy were 
f oimd ; the pelves of both kidneys were dilated, and there was some 
secondary nephritis. The liver was of normal size, rather dark in 
colour, but otherwise seemed perfectly normal. The gall-bladder 
was filled with golden-yellow bile, and on opening it eleven small 
calculi were foimd, the smallest about the size of a pin's head, the 
largest measuring 3'6 mm. x 2 mm. They were angular in shape, 
dull black in colour, and easily friable on pressure. Adherent to 
some of these little calculi and entangling them was thick viscid 
material, apparently inspissated bile, probably with some mucus. 

Three of these calculi, rather smaller than the largest mentioned, 
were foimd impacted in the common duct about 1*5 cm. above the 
duodenal opening. They did not completely block the duct, 
apparently, as bile could be squeezed through from the gall-bladder ; 
but as this was tried before opening the bladder, it was possible, 
though I think very unlikely, that these calculi had been driven 
there by pressure during this examination. So far as could be 
ascertained from a careful examination of one of the minute frag- 
ments, they contained no cholesterin, but consisted mainly of bile 

Casb 2. — May T — , aged 8 months, was admitted under the 
care of Dr. Barlow with cerebral symptoms of five days' duration. 
The child had been ailing since measles two months previously, and 
died two days after admission. The history was very incomplete : 
but no mention was made of jaundice or of abdominal pain. The 
child had been breast-fed imtil one month before admission, and 
since then some patent food had been given. 

Post-mortem. — There was acute miliary tuberculosis, with tuber- 
cular meningitis. The liver showed numerous grey tubercles on its 
surface and in its substance, but otherwise seemed normal. The 
gall-bladder contained some golden-yellow bile; near its neck 
there was a small area about 3 mm. in diameter where the mucous 
membrane showed superficial erosion, and adherent to this was 
some thick mucus, entangled in which was one of the minute calculi 
shown. Only three of these minute concretions were present, and 
inasmuch as they are barely the size of a pin's head, they are hardly 
worth calling calculi, but are of importance only as showing the 
tendency to formation of calculus. They were too minute to allow 
of any satisfactory chemical examination. 

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Oasb 8. — Henry C — , aged 6 months, was admitted imder Dr. 
Barlow for vomiting and wasting of thi*ee months' duration. Some- 
times he seemed to have pain in the abdomen, screaming and drawing 
up his legs. The bowels were costive, there was much straining at 
stool, which was of a pale colour. Breast milk had been given 
until three months ago, then boiled milk with water (equal parts). 
There was no history of jaundice. 

On admisHon the child was emaciated, with sunken eyes and 
depressed f ontanelle ; the abdomen was retracted ; the liver was felt 
one and a half fingers' breadths below the costal margin in the 
right nipple line ; there was no jaundice. A few rales and rhonchi 
were heard over the lungs; the heart was normal. There was 
occasional vomiting; diarrhoea supervened; the child wasted and 
became more exhausted, and died four weeks after admission. No 
abdominal pain was observed. 

Po8t' mortem. — There was slight broncho-pneumonia. The liver 
appeared perfectly normal both to thp naked eye and on microscopic 
examination. The gall-bladder was moderately full of rather dark 
amber-coloured bile, and in the fundus of the bladder were three 
small calculi, the largest being about the size of a millet seed, 
measuring nearly 3 mm. x 2 mm. and being roughly oval in shape 
with roimded contour, not angular. The colour was a dingy black, 
the consistence was very hard, but they were friable under con- 
siderable pressure. No calculi were found in the liver substance. 
Examination of one of these calculi showed no trace of cholesterin ; 
the stone seemed to be made up almost entirely of bile pigment 
associated apparently with some carbonate, as a few bubbles of gas 
escaped on adding an acid. 

A fourth case is perhaps worth mentioning in this connection, 
for although no gall-stones were seen, it appeared from the clinical 
symptoms to be one of biliary calculi. A boy, aged ten years, 
recently came imder my observation suffering from attacks of 
abdominal pain at intervals of a few months. About six years ago 
he was admitted under the care of Dr. Barlow for severe abdominal 
pain with vomiting and jaundice. A fluctuating tumour could then 
be felt in the position of the gall-bladder, and indeed it was thought 
that it might be the distended gall-bladder. The swelling suddenly 
subsided, the jaundice passed off and the child seemed well, but 
since then has had repeated attacks of abdominal pain which last 

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about lialf an hour, and are referred to the umbilicus. During 
these attacks the mother says the boy is of a sallow colour, but it 
seems doubtful whether he is actually jaundiced. The liver is now 
slightly enlarged, and feels firmer than normal. The diagnosis of 
biliary colic seems at least probable in this case. 

Here, then, are three cases in which gall-stones were actually 
found in children, and other similar cases have been recorded. I 
have been able to find altogether twenty published cases ^ in addi- 
tion to those recorded here. 

Of the twenty-three cases thus collected, ten were in infants who 
were stillborn or died within a few weeks of birth ; one is simply 
stated to have been " an infant ; ** four were between three months 
and nine months of age ; and eight were in children from about 
three to fourteen years old. In all these cases the calculi were 
actually seen, in four cases in the faeces during life, in the rest at 
the autopsy. 

Of the ten cases which occurred in newborn children, seven are 
stated to have been jaundiced, and in most of these the jaundice 
was present at birth. Abdominal pain, apparently of the nature of 
colic, was also present in some of these cases, but not in all. 

In one case (Bouisson) some narrowing of the ductus choledochus 
was also found ; in another (Cuffer) the gall-bladder appeared to be 
shnmken. A tendency to haemorrhage was also associated with the 
latter case ; hflematuria and haemorrhage from the bowel were pre- 
sent during life, and haemorrhage into the psoas muscle was foimd 
after death. The jaundice in these new bom infants was very in- 
tense, and in five of the cases was shown post mortem to be due to 
impaction of calculi in the bile-ducts. It is evident, therefore, that 
biliary calculus must be reckoned amongst the causes of icterus 
neonatorum of a severe and persistent variety, which in some cases 
at least ends fatally. 

The presence of gall-stones in later infancy and in childhood has 
rarely been associated with any distinctive symptoms during life. 
The occurrence of jaimdice with colic was recorded only in one 
(Walker) of the thirteen cases, while in another (Case 8) it was 

^ Only CA8C8 in which the gall-stones were actually seen are included in these 
Ktatistics, and only those which occurred not later than fourteen years of age. 
Several other cases are on record where colic, supposed to be biliary in origin, 
occurred in childhood {vide Mercat» *' Colique H^patique chez I'enfant," ' Th^e 
dc Paris,' 1884). 

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especially stated that the child had screamed much and drawn up 
its legs as if in pain. In the remainii^ eleven cases no special 
symptoms of calculus were recorded. It is to be remembered, how- 
ever, that five of these thirteen cases occurred in infancy, when pain 
in the abdomen is so apt to be overlooked or to be attributed to 
such common causes as flatus or dyspepsia, and it is quite possible 
or even probable that some pain may have been present in other 
cases besides the two in which it was mentioned. At any rate, both 
in the new-bom and in these older cases definite abdominal pain 
was sometimes observed, and it seems almost certain that the im- 
paction of calculi in the ducts, as in Case 1 recorded above, or even 
the passage along the ducts of such calculi as were found in Case 3, 
must be attended with some degree of pain. 

I lay some stress on this point because these little biliary concre- 
tions are much more common in early infancy than at any other 
period of childhood, and it is quite possible that biliary colic may 
be the cause of some of the obscure screaming attacks with drawing 
up of the legs which are so common in infancy, and which are 
sometimes so difficult to assign to any definite cause. The pasdage 
of calculi along the bile-ducts, like the passage along the ureters of 
the uric acid concretions, which one finds so often in the infantile 
kidney, is certainly aii occasional cause, perhaps a more common 
one than we suspect, of colic in infants. 

As regards the setiology of gall-stones in childhood, one point 
seems to be of special importance, namely, the much greater 
tendency to formation of gall-stones during early infancy than in 
later childhood. Fifteen out of the twenty-three cases collected 
here were infants, and fourteen of these were imder the age of ten 
months ; and this preponderance of infants seems to be independent 
of sex. Of seven infants in whom the sex were recorded, four were 
males, three were females. Further, as Dr. John Thomson has 
pointed out, it seems quite certain that in many, if not in all, of 
the new-bom cases the calculi have actually been formed during 
intra-uterine life. 

It would appear, therefore, that some condition is present during 
intra-uterine life and early infancy which particularly favours the 
production of biliary concretions. This condition is perhaps to be 
foimd in the tendency to stagnation of bile in the gall-bladder, 
which seems to exist at this period. In making a considerable 
number of autopsies on infants it has struck me, as it seems to 

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have struck several of the writers on the anatomy of childhood, 
that the bile in the gall-bladder is often very viscid in early 
infancy, and such a viscidity would naturally favour, if, indeed, it 
be not the result of, stagnation. 

That a mechanical hindrance which causes stagnation of bile 
may be associated with the formation of calculus is shown by the 
case quoted above, in which a narrowing of the common duct was 
associated with the presence of calculi. 

Moreover, a potent cause of stagnation must exist in the mus- 
cular inactivity of this period ; the contractions of the diaphragm 
in particular are probably completely in abeyance during intra- 
uterine life, and the general movements of the body are extremely 
slight. To a less degree, in extra-uterine life also, the feebleness of 
muscular activity, especially in the weakly infants in whom these 
calculi have been found, must favour the formation of biliary con- 
cretions. April 4ih, 1899. 

4 1 . Syphilitic stricture of bile-ducts, {Card specimen.) 
By W. S. Lazarus-Bablow, M.D. 

IIhe body from which the present specimen i was obtained was that 
- of a boy aged 17 years. He was the subject of well-marked 
congenital syphilis, for which he was treated as an in-patient of 
St. George's Hospital in 1898. On the present occasion he was 
admitted for intense jaundice and weakness of gradual onset of 
several weeks* duration. Liver and spleen much enlarged; no 

After treatment in hospital for two months, during which he 
suffered from vomiting at frequent intervals, though the jaundice 
improved somewhat, the patient died from erysipelas, to which on 
this, as on the previous admission, he had shown an extreme 
susceptibility. The erysipelas was complicated by recent peri- 

At the autopsy the body was extremely emaciated, and was of an 
olive-green colour. Nodes were present on the skull bones and the 
^ St. George's Hospital Museum, series ix, 191b. 

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left tibia. There was a small quantity of bile-stained fluid in each 
pleural cavity and in the peritoneal cavity. The lungs were normal. 
Except for a fine recent pericarditis the heart was normal. The 
alimentary tract was normal except for a perforation of the hard 
palate ; the intestinal contents were devoid of bile-pigment. The 
other organs, with exception of liver and spleen, were normal. 
None of the organs gave the lardaceous reaction. 

Liver aiid bile-passages, — The liver weighed 5 lbs., was of a dark 
green colour from retained bile, and was almost entirely constituted 
by an enormously hypertrophied left lobe, which was normal in its 
composition. The right lobe was very small, and showed numerous 
cicatrices and depressions, the seat of old gummata. One mass of 
fibrous tissue of this description especially involved the bile-ducts, 
but its major portion lay on the dorsal surface of the organ. The 
gall-bladder was of normal size, and full of dark green bile. The 
common bile-duct and the left hepatic duct were each the size of a 
No. 16 catheter ; the ampulla at the blind end of the common duct 
was the size of a hazel nut. The left hepatic duct was not only dilated, 
it was also separated from the common duct by a thin but perfect 
membranous septum. There was some difficulty in deciding the 
position of the right hepatic duct, but it is apparently represented 
by a depression into which the tip of a small probe will enter, and 
situated in a small diverticulum in the ampulla at the blind end of 
the common duct. The author suggests that the bile found in the 
gall-bladder may have been derived from the atrophied right lobe 
of the liver through this stenosed right hepatic duct ; it appears 
impossible that it should have been derived from the left lobe. 
The occlusion of the left hepatic duct is sufficient explanation of 
the severe jaundice which obtained. A gall-stone (bilirubin- 
calcium) was present in the dilated common duct, but did not in 
any degree occlude it. It was probably formed in the ampulla, 
judging from its shape and size. The spleen weighed 2 lbs. 13 oz.; 
it was much firmer than normal, but presented no special features 
beyond its size. May 16th, 1899. 

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42. Tuberculous cavities in the liver. 

Bj Herbert Morley Fletcher, M.D., M.R.C.P. 

[With Plate IV.] 

IT is somewhat remarkable that so little notice of this form of 
hepatic lesion should have been taken in this country ; in fact 
it is difficult to find any reference to it, whereas it has been freely 
described by foreign writers for many years past. 

Judging by the number of cases quoted by French and German 
authors, the condition appears to be of more frequent occurrence 
abroad than it is in this country, though in all probability it is not 
of such great rarity here as might be supposed. 

The history of the case is briefly as follows : 

The patient was a boy aged 6, who was under the care of Sir 
Dyce Duckworth at St. Bartholomew's Hospital. 

He was admitted in September, 1898, in an unconscious condition. 
He had been in his usual health till three days previously ; he then 
became irritable, had severe headache, and rapidly grew worse. 
There was no jaundice. 

He died the day after admission. The clinical symptoms pointed 
to its being an extremely rapid case of tuberculous meningitis, the 
duration of symptoms being less than a week. There was no family 
history of phthisis. For some months past the boy had suffered 
from repeated attacks of diarrhoea. He had had measles, but no 
other illness. 

Post-mortem examination. — The ;post-mortem, made by Dr. Garrod, 
showed that the case was one of general tuberculosis. There was 
tuberculous meningitis. The lungs and pleurse contained miliary 
tubercles. There was a large caseous bronchial gland attached to 
the right bronchus. The intestines and omentum were covered 
with tubercles. The jejunum and ileum contained many tuber- 
culous ulcers, and there were a few in the large intestine. The 
spleen and kidneys contained miliary tubercles; the pancreas, 
supra-renals, ureters, and bladder were normal. The liver weighed 
23 oz. The gall-bladder was natural and contained bile ; the ducts 
were patent and were not dilated. There were many miliary 
tubercles in the substance of the liver, and a few under the 

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Illustrating Dr. H. Morlej Fletcher's paper on Tuberculous 
Cavities in the Liver. (Page 160.) 

Fio. 1.— A tuberculous cavity in the liver. The wall of the cavity is composed 
of dense, well-developed fibrous tissae, in which are embedded several giant cells. 
Within this is a partially caseous sone containing the remains of a bile-duct. In 
the centre is a mass of dark-brown, bile-stained, granular dihrit, 

Fio. 2.-»To show an earlier stage in the formation of a cavity. There is a 
capsule of fibrous tissue enclosing a typical tubercle. The outer part of the 
tubercle contains several giant cells. In the central caseous portion is a partially 
destroyed bile-duct. 

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capsule. Some of these, especially those under the capsule, had 
the ordinary grey translucent appearance. The majority of those 
in the liver substance were larger, and had a distinctly green tint, 
the green colour being chiefly confined to the centre of the tubercle. 

In addition to these miliary tubercles there were numerous 
cavities, each about the size of a large pea. They were enclosed by 
a thick, white capsule, and filled with bile-stained debris. In some 
. instances the contents of these cavities had a metallic lustre 
(?cholesterin). No communication between the cavities and the 
bile-ducts could be made out at the post-mortem. The liver tissue 
was congested, but showed no other naked-eye change. 

Microscopical examination. — Sections showed the presence of 
tubercles of obviously different characters. There was a com- 
paratively small number of quite recent miliary tubercles under 
the capsule and within the lobules. These presented the usual 
features of tubercles associated with an arterial infection, and were 
obviously of quite recent date. They were quite small, and showed 
ittle or no signs of caseation. 

In addition to these there was a far greater number of larger 
tubercles situated in the portal canals. They exhibited very exten- 
sive caseation, and were surrounded by a thick, well-developed 
fibrous capsule. Many of these larger tubercles were bile-stained. 
In some of these in the central caseous area could be made out the 
remains of a bile-duct, the wall of which has been broken down. 
This is well shown in the drawing (fig. 2, Plate IV). The remain- 
ing epithelium of the duct can be seen partially detached. Near 
the periphery are numerous giant-cells, and surroimding the 
tubercle is a well-defined fibrous wall. This illustrates an early 
stage in the formation of the cavities. Later, when caseation has 
further advanced, the bile-duct becomes completely destroyed, and 
a cavity is produced filled with bile-stained debris. This can be 
seen in fig. 2. 

The wall is composed of dense fibrous tissue forming a complete 
investment, and embedded in it are a few rather shrunken giant- 
cells. Within this is a narrow zone of small round-cells, in which 
may be seen a proliferated bile-duct. This surrounds a large cavity 
filled with granular dark brown debris, 

A large number of sections from different parts of the liver were 
<;ut in order to fully investigate the changes in the bile-ducts them- 
selves. In many places there was distinct evidence of cholangitis, 


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as shown by the swelling and proliferation of the epithelium, but it 
was found that these changes were almost invariably associated 
with the presence of a tubercle in the immediate vicinity of the 
duct. There was little, if any, evidence of a generalised or diffuse 
inflammation of the ducts. Sections stained to show tubercle 
bacilli gave a positive result. 

Remarks. — As has been previously stated, very few similar cases 
have been described in this country. 

Dr. Wethered, in 1889, showed at the Pathological Society a liver 
containing similar cavities with bile-stained contents, some as large 
as a chestnut, which was obtained from a man aged twenty one, who 
died of general tuberculosis. In this case there was tuberculous 
peritonitis. Dr. Wethered regarded it as a case of primary tuber- 
culosis of the liver, though I have little doubt that it was one of 
tuberculous cholangitis. 

Dr. H. Mackenzie, in 1890, brought before this Society a case in 
a man aged twenty, probably of the same nature, which he described 
as tuberculous disease of the liver, with the formation of multiple 
abscesses. He regarded an old ulcer which was present in the 
small intestine as the probable source of infection of the liver. 

Many cases of these cavities in the liver have been described by 
foreign authors. Cruveilhier, who was one of the first to mention 
them, regarded the cavities as due to simple dilatation of the ducts, 
and called them biliary cysts. He did not recognise their tuber- 
culous origin. Rilliet and Barthez, Orth, Arnold, Virchow, and 
others described similar cases, and showed that the cavities were 
the results of deposition of tubercle in the liver. Rilliet and 
Barthez in particular compared them to cavities in the lung pro- 
duced by tubercles breaking into the bronchial tubes. They also 
state that in seventy-six cases of tuberculosis of the liver these 
cavities were present in forty-six. Other cases have been recorded 
by Toupet, Gaucher, Quinquand, &c. 

The first minute investigation into the mode of formation of 
these cavities was that of Sabourin in 1883, who was the first to 
recognise the presence of cholangitis. He maijitained that the in- 
fection reached the liver by the blood, that tubercles were formed 
in the portal spaces, and might burst into the bile-ducts, or, as he 
expressed it, the ducts are infected from without inwards. 

Three cases, in patients aged sixteen, seventeen, and fifty-eight 
years respectively, are described by Kotlar in an admirable paper. 

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In this he holds that the lesions are not due to a tuberculous cholan- 
gitis, but that the infection is hflematogenous, and that the cavities 
are due to caseous degeneration in a caseous nodule, the bile-duct 
being secondarily involved. 

Sergent, in 1895, confirmed these views of Sabourin's by experi- 
mental observation. He showed that inoculation of the portal vein 
leads to a non-systematic infection of the bile-ducts passing from 
without inwards. Inoculation of the common bile-duct causes a 
systematic tuberculosis of the biliary canals, which passes from 
within outwards. He further showed that the tubercle bacillus is 
unaffected by bile, and that the bile taken from various cases of 
tuberculous cholangitis contained tubercle bacilli. Somewhat simi- 
lar experiments made by Gilbert and Claude show similarly that 
tuberculous infection of the bile-ducts can readily be produced in 

In short, we may roughly divide the writers on this subject into 
two classes : those who hold the view that the primary cause of a 
cavity is the formation of a tubercle in the portal space secondarily 
involving a bile-duct, and those who believe that the lesion is due 
to a biliary infection with resulting tuberculous cholangitis. 

The possible channels by which tubercle bacilli may reach the 
liver, are the hepatic artery, the portal vein, the lymphatics, and 
possibly the bile-ducts. To these we must add the umbilical vein 
in the foetus. The most common variety of hepatic tuberculosis is 
that in which, as the result of an arterial infection, bacilli are con- 
veyed to the liver by the hepatic artery, and produce the common 
variety of miliary tuberculosis. 

In the liver I have described, it is more than probable that some 
of the small, recent, non-bile-stained tubercles have been produced 
through this channel. This is, however, evidence, I think, that in- 
fection has been brought about through the portal vein, from the 
situation of the tubercle in the portal canals, and their close corre- 
spondence with those produced by experiment. This infection is 
probably the result of the lesions in the intestines, which were of 
comparatively long standing. The tubercles found in the portal 
canals are certainly of greater age than those occurring in the 
lobules and under the capsule. There is evidence in sections of the 
Uverthat some of these tubercles have brought about a destruction 
of the walls of the bile-duct adjacent to them, so that their caseous 
contents have been in free communication with the lumen of the 
duct. This is entirely in accord with the views of Sabourin and 

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Kotlar, and with the experimental work of Sergent, that in dogs 
inoculated by the portal vein, infection of the bile-ducts occurs from 
without inwards. This will account, I think, for the formation of 
some, at any rate, of the smaller cavities in this liver. 

It is interesting to note that in many of the recorded cases of 
tuberculous cavities in the liver, ulceration of the intestine was 
present. In some of the others there was tuberculous perito- 

We have next to consider whether the infection may have arisen 
by the lymphatics. This is highly improbable, as the current of 
lymph in the lymphatics of the liver is towards the hilum, so that 
infection brought to the liver by the lymphatics is directed against 
an opposing flow. Such infection, if it occurs, must be of extreme 
rarity. Further, as Sergent showed in cases where artificial tuber- 
culosis of the bile-ducts had been established in dogs by inoculation 
of the bile- ducts, and also in cases of tuberculous cholangitis in 
man, he invariably found an infected gland at the angle between 
the common duct and the pancreas, — a further evidence as to the 
direction of conveyance of the bacilli. 

Lastly, is there evidence of infection by the bile-ducts ? The 
larger bile-ducts are probably rarely, if ever, infected from the 
intestine, and in this case it is extremely improbable that this had 
occurred, as they were apparently quite normal. Sergent, by his 
experiments, showed that tubercle bacilli were unaltered by bile, 
and retained their virulence, and, with other writers, considered 
that these cavities were associated with cholangitis of tuberculous 
origin. In the case I have described there is no evidence of a 
general cholangitis, nor is there conclusive evidence of this in the 
cases described previously. The bile-ducts appear to be affected 
locally, and in the neighbourhood of a tubercle. It is noteworthy 
that in none of the recorded cases that I have found is the occur- 
rence of jaundice mentioned. 

In conclusion I agree with Kotlar, that the lesions are not due to 
tuberculous cholangitis, and that this term is a misnomer. At the 
same time we must recognise the possibility of cholangitis being 
secondarily set up by the discharge of tuberculous material into the 
ducts during the process of formation of the cavities. This secondary 
oholangitis is to be found in the liver I have examined. In places, 
generally near a tubercle, the epithelium of the duct may be found 
swollen, proliferated, and undergoing desquamation, the canals in 

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some places being filled with the products of degeneration. In 
other parts the ducts are apparently quite normal. 

A considerable length of time has probably been necessary to 
produce the cavities of dense fibrous tissue— at least several months 
— as after three months Gilbert showed experimentally in dogs the 
cavity formation had not occurred, the animals dying before their 
proper development. 

We may sum up the sequence of changes present in the liver as 
follows : — A quite recent arterial infection by the hepatic artery ; an 
older infection through the portal vein, probably associated with 
the intestinal lesions, and resulting in the formation of tubercles in 
the portal spaces. 

Next, a destruction of the walls of the bile-ducts, with formation 
of a cavity filled with bile- stained caseous material; and secon- 
darily, the production of localised cholangitis. 

In conclusion, I must tender my thanks to Sir Dyce Duckworth 
for allowing me to publish this case, and to make use of the Ward 


Arnold. — * Virchow*8 Archiv,* Bd. Ixxxiii, s. 377. 
CruveilAier. — * Anatomie pathologique g^n^rale,* tome iv, pp. 839 — 841. 
Gaucher.—* Bull. Soc. anat. de Paris,' 1879, p. 545. 

CHlbert ei Claude.—* Compt. rend. Soc. de Biol.,' Paris, 1895, pp. 841—844. 
ITotlar.—* Zeitschr. f . Heilk.,' Berlin, 1894, Bd. xv, S. 121. 
Mackenzie. — 'Trans. Path. Soc. Lond.,' vol. xli, p. 156. 
Or^A.— ' Virchow's Arcbiv,' Bd. Ixvi, p. 118. 

Silliet et Barthez.—* Maladie des finfants,' Srd edition, 1894, vol. iii, p. 1273. 
Sabourin. — * Arch, de physiol. norm, et path.,' Paris, 1883, p. 52. 
Serffent.—* Compt. rend. Soc. de Biol.,' Paris, 1895, pp. 336 and 351 ; • Thhse 
de Paris,' 1896. 

Toupet.-^' Bull. Soc. anat. de Paris,' 1886, tome Ixi, p. 647. 
Wethered.—'TmnB. Path. Soc. Lond.,' vol. xl, p. 189. 

January 17 th, 1899. 

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43. A case of carcinoma of the liver believed to have been 
primary in that organ. 

By Chablbs D. Grbbn, M.D., F.R C.S. 

THB specimen consists of portions of liver taken from tte body of 
a woman who at the time of her death was 54 years old, and 
who died after several months' illness. 

The organ is seen to be very extensively invaded by a malignant 
growth having its centre in the right lobe ; the growth has reached 
the capsule on the convex surface of the liver and to a less extent 
on the under surface and at the free border ; the central portion of 
the growth has undergone fibrous transformation, and is tough and 
dense ; blood-vessels, which are still patent, can be seen in it. The 
disease has extended from the main growth by the development of 
numerous secondary nodular tumours, which can be seen surround- 
ing it ; they vary considerably in size ; the more recent and outlying 
of them have remained discrete, but those nearer the main mass 
have to a great extent coalesced. In the peripheral portions of the 
main mass are a few small patches of congestion, and several of the 
secondary nodules show a white central portion bounded by a 
narrow vascular or heemorrhagic zone, beyond which the growth 
shades off without any clear line of demarcation into the surround- 
ing liver tissue. The liver substance in places is of a dark green 
colour from distension of the biliary capillaries, but this appearance 
was shown over only a comparatively limited area ; elsewhere the 
liver substance between the growths was of a pale colour and rela- 
tively soft consistence, suggesting fatty change. 

The glands in the portal fissure are enlarged and infiltrated by 
the growth, but have not coalesced ; they are preserved attached to 
the specimen with the common bile-duct and a portion of the 
pancreas and of the duodenum. The bile-duct is not distended, and 
appears to have been only partially obstructed. The gall-bladder is 
contracted rather than otherwise, is not involved in adhesions, and 
shows no signs of new growth ; there is no evident infiltration of 
the connective tissue of the portal fissure. 

About a third of the left lobe of the liver was free from any 
large mass of new growth, but even here there were several small 

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scattered nodules. The larger portal canals appear thickened, but no 
such appearance is noticeable about the hepatic veins. Histolo- 
gically the grovrth is a carcinoma showing much varietj of 
structure in sections taken from different parts. 

In the central portion of the growth fibrous transformation has 
taken place, and the cellular elements are few ; the epithelial cells 
have a distinctly polygonal outline. In many places the bands of 
fibrous tissue can be seen to radiate from islands of dense connec- 
tive tissue ; these I take to be the remains of portal canals from 
which vessels have in many places disappeared ; in some of these 
bands of fibrous tissue long columns of epithelial cells can be seen, 
in some instances unbranched for comparatively long distances, 
in others branching in a manner recalling the ramifications of 
vessels. There are in places large arece of what appear to be 
degenerated liver cells ; there are also seen cells with a large 
spheroidal nucleus and containing pigment granules. The cancer 
cells in the dense fibrous tissue of the central portion are smaller 
than those seen elsewhere, and appear to be undergoing atrophy. 

In sections taken through one of the secondary discrete nodules 
several different appearances can be seen : 

1. A central zone where considerable development of fibrous 
tissue has taken place, and where the active cellular elements are 
relatively few ; columns of epithelial cells can in places be seen as 
above described ; the liver tissue where recognisable is undergoing 
necrotic change. 

2. A narrow zone of vascular congestion, in the vicinity of which 
is — 

3. The more typically carcinomatous zone. This shows in places a 
fairly perfect alveolar structure, in others the cells are in masses 
without definite arrangement. The cells are for the most part 
definitely polygonal ; they stain deeply with heematoxylin ; in some 
places the cells have a trabecular arrangement. Here and there are 
granules of bile pigment. 

4. The margin of the growth shading off without definite boundary 
into the surrounding liver substance, which shows much fatty change. 
A section taken from one of the affected lymphatic glands shows 
the same tendency to the trabecular arrangement of the cells and 
to the formation of necrotic arese that is seen in the main growth, 
and the cells have the same polygonal outline. 

Sections of the liver substance taken from beyond the visible 

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limits of the growth show much fatty change, with some increase of 
fibrous tissue in the portal canals, but without annular cirrhosis. 
The epithelium of the bile-ducts shows up very distinctly. Nearer 
the growth the increase of fibrous tissue in the portal canals is 
much more marked, and shows some admixture of epithelium. 

Sections of the pancreas showed no distinct evidence of new 

At the autopsy no other new growths were found ; there was a 
small patch of recent inflammatory deposit on the upper surface of 
the liver, and the duodenum was loosely adherent for about half an 
inch to its under surface. There was no ascites. 

The spleen showed no obvious change. 

The kidneys presented some narrowing of their cortex, and the 
capsules were slightly adherent No other lesion of importance 
was detected in the body. 

The whole length of the intestine was not slit up, and permission 
to make the examination having only been granted subject to the 
condition that the head should not be opened, the state of the 
brain could not be ascertained. 

The examination was made under circumstances of some difBculty. 

The clinical history of the case is as follows : — I had known her 
for some years prior to her death, but until the present year she 
had shown no sign of serious illness. There was no history of 

She came to me twice in December, 1897, complaining of head- 
ache and giddiness, but I did not see her again until July 2 1st, 
1898, when she came to me complaining of frequent and obstinate 
vomiting ; it was then quite evident that there was considerable loss 
of flesh and general deterioration of health. No abnormal physical 
signs were detected on examination, and the urine was free from 
albumen and from sugar. It seemed probable that she was suffer- 
ing from malignant disease of stomach. 

The vomiting was not persistent, but occurred in paroxysms at 
varying intervals, and was generally accompanied by headache and 
giddiness ; there was no optic neuritis, no paralysis, nor any direct 
evidence of cerebral mischief. Constipation was a prominent s>Tn- 
ptom throughout. 

She continued to get weaker, but no definite diagnostic indignation 
of the seat of disease occurred until early in September, when she 

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began to complain of pain localised in the right side and aggm- 
vated by deep inspiration. A friction sound conld soon afterwards 
be heard at the right base, which persisted for about ten days and 
could then be no longer heard ; the pain, however, did not abate. 
There was also about this time some epigastric tenderness. 

During the last week in October an ill-defined swelling could be 
felt, apparently connected with the liver, just bflow the ribs, a 
little to the right of the middle line, and this persisted and seemed 
to increase in size, but no definite limits could be assigned to it. 

There was never any evidence of ascites, but the abdomen was 
somewhat distended during the last few days of life, owing to 
gaseous accumulation in the bowels; there was slight jaundice 
noticed for fourteen days before death. 

Death took place on November 26th from very slowly progres- 
sive nutritional failure. 

The only noteworthy feature found at the autopsy besides the 
conditions described in connection with the specimen was that there 
was no trace of recent pleurisy ; the pain and friction must there- 
fore have been due to the growth reaching the capsule of the liver 
on its convex surface. 

We have here a groyrth which has destroyed the greater part of 
a large and important organ, but beyond infiltrating a few lym- 
phatic glands in its immediate vicinity has given rise to no secondary 
deposits. It has thus shown great local malignancy and but little 
tendency to dissemination. The central portions have undergone 
fibrous transformation and atrophy, perhaps similar to what occurs 
in atrophic scirrhus of the breast, and this tendency is exhibited 
not only by the main growth but also by the outlying nodules ; the 
clinical history and the post-mortem appearances both point to a 
slowly growing tumour. 

I think the absence of calculi, the apparently normal condition of 
the gall-bladder, and the absence of columnar epithelium in the 
lymphatic glands, together with the late appearance of jaundice, 
are facts pointing against the disease having originated in the gall- 
bladder or in the main bile-ducts ; there is, it is true, some approach 
to the short columnar type in some of the cells in certain places in 
the growths in the liver, but this may well be due to irritation of 
the bile-ducts by the development of the disease and their secondary 
participation therein; besides, polymorphism is not unknown in 
oArcinomatous growths. 

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The total absence of ascites and the fact that there was no en- 
lai^ment of the spleen practicallj n^ative the hypothesis of cancer 
following upon cirrhosis, and the appearance of the sections of liver 
taken from well beyond the visible limits of the growth showing 
but little development of fibrous tissue is also against this view. I 
therefore think that in this case the growth originated in a morbid 
activity, beginning in the liver cells themselves. 

MM. Hanot and Gilbert, in writing of primary carcinoma of 
liver in their work on diseases of that organ, remark : " C*est la 
cellule hepatique, c'est k dire Tel^ment noble du foie, qui fait tons 
les frais de la metamorphose; les autres elements ou bien dis- 
paraissent par atropine, ou bien concourrent seulement a la formation 
du stroma." 

Dr. Bolleston, in his paper on malignant disease of the gall- 
bladder and bile-ducts, published in the * Clinical Journal ' of April, 
1897, says that carcinoma beginning in the bile-ducts is almost 
always columnar-celled, and mentions progressive jaundice usually 
lasting about six months as one of the symptoms. 

In a case of my own, which was probably primary in the gall- 
bladder, there was a large carcinoma involving the liver, the colon, 
and the stomach, and which was associated with a single large 
calctdus. The secondary nodules in the liver showed groups 
of epithelial cells, the peripheral layer of which was distinctly 
columnar, and the central layers were spheroidal and flattened, 
with, in places, tendency to the formation of nests so commonly 
seen in surface epitheliomata. 

Hanot and Gilbert, in the work above quoted, speaking of the 
affection of the interstitial tissue in cases of primary cancer of the 
liver, say : " Le tissu interstitiel est le siege de lesions inflanunatoires 
etendues a la totality du foie. Dans le cancer trabeculaire Ton 
constate presque toujours Texistence d'une cirrhose veritable. 
Celle-ci parfois insulaire presque toujours annulaire se fait re- 
marquer frequemment par le grand nombre de canalicules biliaires 
dissemin^s ou agmines en plaques qui criblent ses jet^es ou ses 
anneaux." January Srd, 1899. 

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44. Atrophied pancreas from case of diabetes melliiw. 
{Card specimen.) 

Bj T. W. P. Lawebncb. 

THE pancreas retains the normal shape and exhibits slight signs 
of lobulation ; but it is greatly reduced in size, measuring five 
inches in length, fiye eighths of an inch in width, and one quarter 
of an inch in thickness. Its weight is 4 drachms 15 grains. The 
specimen was presented to the Museum of Universitj College 
by Dr. Henry J. Price, of Maldon, Essex, and was taken from a 
single woman aged 32, who was suffering from diabetes mellitus 
and who had been under treatment for six months before her death. 
The daily excretion of urine varied between three and five pints. 
The normal acini of the gland are not recognisable under the 
microscope, and their place is taken by masses of granular material 
in which nuclei are visible in places. There is considerable increase 
of the fibrous tissue of the gland, and the vessels exhibit marked 
fibroid degeneration. April Mh, 1899. 

45. Primary columnar-celled carcinoma of the tail of the 
pancreas. [Card specimen.) 


CLINICAL Abstract. — A woman aged 49 years was admitted 
with great pain in the back and abdomen. She was thin and 
distinctly pigmented, but no trace of jaundice was ever present. 
There was no glycosuria. A projection was felt in the back to the 
left of the spine at the level of the ninth dorsal vertebra ; nothing 
could be felt in the abdomen. After she had been in a week she 
had an epileptic fit, and a week later her mind became deranged 
and she refused to speak. Two days later small tumours were felt 
under the skin of the right thigh over Hunter's canal and on the 

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perineeum. Five days later she died. Tlie diagnosis was primary 
malignant disease of the spine. 

Post-mortem examination showed a primary growth on the tail 
of the pancreas close to the spleen. The growth was white in 
colour, fairly firm in consistence, and had begun to eat its way into 
the capsule of the left kidney. Several of the branches of the 
splenic artery were compressed and obstructed by the growth. The 
splenic vein was thrombosed, and the thrombus extended into the 
portal vein. The spleen contained a number of recent anaemic 
infarcts. Microscopic examination showed the absence of any 
trace of growth in the infarcted areas. The adrenal bodies were 
free from growth. The oesophagus, stomach, and intestines were 
normal. There was no fat necrosis. There were secondary growths 
in the pleurae, in the liver, in the muscles of the back opposite the 
ninth dorsal vertebra, and in the subcutaneous tissue of the right 
thigh and perinseum. There was an old clot in the aorta near its 
bifurcation, and in the left common iliac artery. There was also an 
adherent thrombus on the left ventricle, and some vegetations on 
the mitral valve. There were pulmonary apoplexies in both lungs, 
and a cerebral haemorrhage into the right external capsule. 

Microscopically. — The growth was a columnar carcinoma. The 
structure was well seen in the secondary growths, in the liver and 
in the muscles of the back. In places there was a transition to a 
spheroidal-celled carcinoma. 

Remarks. — The following points are of interest : 

(1 ) Situation of the growth. While the tail of the pancreas is 
said to be the commonest part of the gland for secondary grovfths 
(Vemay), it is a rare one for a primary neoplasm* Mirallie, in his 
digest of 113 imdoubted cases of primary carcinoma of the pancreas, 
only refers to one instance (Laennec's) of the disease arising on the 
tail. Norman Moore in his collection of cases says that the 
duodenal end was always the part affected. Lancereaux, however, 
says that in fifteen cases observed by him, the tail was affected in 
two. Ebstein has recently reported a case of latent carcinoma of 
the tail of the pancreas. A case recorded by myself in the * Trans- 
actions ' of this Society (vol. xliv, p. 820), of carcinoma of the tail 
of the pancreas with a secondary growth in the anterior medias- 
tinum, is open to the objection which I now share, that the growth 
was primary in the thymus gland or its remains, and that the 
pancreatic growth was secondary. 

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(2) The nature of the growth. Carcinoma of the pancreas is 
nearly always spheroidal-celled. Bard and Pic described columnar- 
celled carcinoma, and pointed out that it was derived from the 
epithelium of the ducts of the gland, carcinoma of the ** excretory 
type " as they called it, or as it would be now termed duct cancer. 
Kuhn recorded a most exceptional case of this histological form of 
pancreatic carcinoma in a girl aged two years. Cases have also 
been recorded by R. Pott and by E. Wagner, but Comil and 
Ranvier consider that the growth in the latter case spread to the 
pancreas from the duodenum. Mr. Beadles described a case of 
columnar-celled carcinoma in the earlier part of this session 
(p. 174). 

(8) The coincidence of an exceptional position for carcinoma of 
the pancreas with an exceptional form of growth. The pancreatic 
duct is so comparatively small at the tail end that the occurrence 
of a duct carcinoma there is remarkable. 

(4) The invasion of the branches of splenic artery by the groyrth 
and the resulting obliteration, which was accompanied by anaemic 
infarcts in the spleen and thrombosis of the splenic vein. 

(5) The general tendency to thrombosis, as shown by the throm- 
bosis in the aorta, the left common iliac artery, and the left 

(6) The fairly wide-spread generalisation of the growths. 

(7) The latency of the primary growth, the secondary groyrth in 
the muscles of the back appearing during life to be the primary. 

Vemay, — * Tb^ de doctorat,' 1884, Lyon (quoted by Mirallie). 

Mirallie.—* Gaz. des hdp.,' Paris, 1893, Aug. 19fcb, p. 889. 

Lctennec, — ' Oaz. m^. de Nantes,' 1892 (quoted by Mirallie). 

N. Moore,— 'St, Bart.'s Hosp. Rep.,' vol. x?iii, p. 205. 

Lancereaux, — ' Traits des Maladies da foie et du pancreas,' p. 844, 1899. 

W, Mttein.—* Dentoche med. Wochenschrift,* Feb. 2nd, 1899, No. 5, S. 71. 

Bard and Pic.—' Rev. de M^d.,' 1888. 

ZSAw.— 'Berlin klin. Wochenschrift,' 1887, No. 27. 

a. FoU.—* Deutsche Zeitscbrift f. prakt. Med.,' 1878, Bd. v, S. 181. 

S. Wagner,— * AtMv d. Heilkunde,' 1861, Bd. ii, S. 286. 

Comil and Ranvier, — ' Manuel d'bistologie patbologique,' vol. ii, p. 490. 

May \Uh, 1899. 

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46. Lesion of the pancreas with fat necrosis. {Card specimen.) 
Bj Cecil F. Beadles. 

IN this specimen necrosis of the peritoneal fat is associated, 
as is commonly the case, with disease of the pancreatic gland ; 
but the latter lesion is of an unusual character, and is itself of 
considerable interest, for in addition to a general fibrosis of the 
organ there is a localised mass of malignant groyrth situated in its 
right extremity, having the microscopical features of columnar- 
celled carcinoma, so that it has doubtless taken origin from the 
wall of the pancreatic duct. 

The patient was a female lunatic aged 62, who had been insane 
for a period of over sixteen years. Her mental state at first was 
that of melancholia, with well-marked aural hallucinations and 
delusions of electricity ; she passed, however, into a state of chronic 
mania with periodical outbursts of excitement and violence ; was of 
an impulsive and threatening nature. Her delusions persisted, and 
she finally became more demented. 

Three months before death she began to get jaundiced. This 
increased, and she had a vague pain in the epigastric region, which 
she was unable to exactly localise. Although no abdominal tumour 
could be detected, it was believed she was suffering from malignant 
disease. Slow and gradually increasing weakness set in, and she 
remained confined to bed. During the last week or two she had a 
sense of nausea, but no vomiting. There was no diarrhoea, and she 
passed no blood either by the mouth or rectum. Bowels acted fairly 
regularly, but the motions were pale in colour. She is not known 
to have met with any injury. 

At death the body was well nourished, the skin jaundiced, and 
all the internal organs deeply bile-stained. Fat on the abdominal 
parietes was two to three inches thick, and appeared of a natural 
character. A considerable excess of fluid existed in the pericardial 
cavity. The cardiac valves were fairly healthy, but the right 
ventricular wall was much thinned and replaced by fatty tissue. 
Bases of both lungs congested. Excess of fluid within the skull. 
The brain softened, choroids deeply bile-stained, but finer mem- 
branes and blood-vessels healthy. Stomach and intestines natural ; 

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spleen slightly enlarged and soft; pelvic organs healthy; both 
kidneys a little enlarged. The liver was large and bile-stained; 
weighed 56 oz. The biliary ducts throughout were greatly dilated, 
and filled with glairy fluid. The gall-bladder contained a dozen 
small calculi and some bile somewhat altered in character. 

The specimen consists of the pancreas, duodenum, left kidney, 
and its surrounding perinephritic fat. This fat differs from that 
elsewhere in the fact that it is of a denser character than natural, 
being pervaded by thick bands of fibrous tissue, which under the 
microscope are seen to be composed of a young and loose form of 
connective tissue. Scattered about this fat are extensive areas of 
necrosis ; they are of an opaque white colour, in parts bile-stained, 
resembling to the naked-eye areas of caseation. This adipose tissue 
formed a thick investing capsule around the left kidney and readily 
shelled out with it, whereas the fat on the right side was natural in 
appearance and not in excessive amount. The right kidney lay free. 

The true capsule of the left kidney is thickened. That organ is 
a little enlarged, its cut surface soft and deeply bile stained, its 
surface granular. There are several small cysts in the cortical 
portion, and these contain dark clotted blood. The pelvis is filled 
with fat. Microscopically the condition of the organ is best de- 
scribed by the term "mixed kidney," meaning thereby a certain 
amount of fatty degeneration of the renal epithelium with an 
increase of the interstitial connective tissue ; there is hsemorrhage 
into this in places. Section through one of the cysts shows a thick 
fibrous wall with deposits of old blood pigment in it. 

In the fresh state the pancreas presented an unnatural degree of 
hardness throughout. The organ is unduly adherent to the sur- 
rounding fat, and is intimately blended to the wall of the small 
intestine, more particularly the lower and inner part of its head 
to the third portion of the duodenum. Section through the length 
of the gland reveals a hard fibrous nature, with considerable dilata- 
tion of the duct; this latter was filled with a nearly colourless 
sticky fluid, so that there was clearly an obstruction to the outflow 
of the glandular secretion. A small area of the gland, less than an 
inch in diameter, where its attachment to the duodenum was most 
marked, is of a firmer and denser structure, and the cut surface of 
this closely resembles that of a scirrhous growth. 

The histological character of this tissue is that of typical carci- 
noma of the columnar- celled variety, that is to say, alveolar spaces 

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lined by cubical or colunmar-sliaped cells, either arranged in a single 
row or massed together more irregularly. This malignant groyrth 
appears to be strictly limited in extent to the small area above men- 
tioned, and does not exist elsewhere in the gland. But sections 
taken from various other parts of the organ reveal changes of an 
abnormal character but which are not of a malignant nature. 

There is throughout the pancreas a condition of fibrosis. An 
overgrowth of fibrous connective tissue, varying in places between 
fuUy-formod fibrous bundles which encircle the lobules, and wide 
bands of young connective-tissue formation. Within these latter 
there are frequently collections of small, round, inflammatory ceUs, 
which present the appearance of miniature abscesses. The proper 
secretory cells of the gland are for the most part largely degenerated, 
either by a process of self -digestion or have passed into a state of 
necrosis. In unstained sections the former are still translucent, but 
the latter appear as small opaque areas : the frequency of these two 
conditions varies in different parts of the gland. 

The malignant growth in this organ, owing to the absence of any 
other gro¥rth in the body, clearly proves it a primary carcinoma of 
the pancreas, and its situation and minute structure suggest that it 
took its origin from the duct of the gland. Further, the exceed- 
ingly limited extent of this malignant deposit, presenting at the 
same time active growth and a rapidly extending margin associated 
with a chronic inflammatory change throughout the entire gland, 
suggests to my mind that the simple chronic changes existed 
primarily, and that malignancy has supervened at a comparatively 
late date, possibly as a result of obstruction to the outflow of the 
secretion or an alteration in the composition of the pancreatic juice. 
In cancer of the pancreas it is not usual to find a general fibrosis 
of the oi^n as a part of the malignant process. 

From the point of view of the fat necrosis, the combination with 
cancer of the pancreas is interesting. This singular lesion of the 
peritonitic fat still requires much light thrown on its aetiology. So 
far, cases appear to have been mostly associated with haemorrhage 
or inflammation involving in some way the pancreatic gland, but 
the true connection between the two lesions has yet to be explained. 
Two recorded cases of this lesion with pancreatic carcinoma are 
those of Newton Pitt* and Mayer ;* the former was a large 

1 'Path. Trans.,' 1894. 

a * Wien. med. Pregse,' No. 1, 1899 (epitome, * Brit. Med. Jn,,' 1899, vol. i,p. 46). 

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carcinomatous f?ro¥rth, the latter "fibrous carcinoma" of the 

But apart from all other considerations, the present specimen is 
of interest from the earlj state of the cancer and the fact that it is 
a columnar or duct variety. 

Brief notes of a second case of peritoneal fat necrosis may be 
worthy of record, as there are points of interest apart from the fact 
that this is the only other instance of the lesion found amongst the 
insane dying in Colney Hatch Asylum since the case recorded by 
myself in the * Pathological Transactions * for 1893. 

A man aged 63 died in July, 1898, from heart disease, having 
been the subject of chronic mania for 84 years. There was much 
superficial fat and a great accumulation of adipose tissue in the 
omentum and folds of the mesentery. Scattered about that of the 
omentum were areas of necrosis. The walls of the stomach were 
thickened, intensely congested within, and adherent externally to 
the spleen, which was hypertrophied and weighed 15 oz. Between 
these organs, and in contact with the pancreas, was an abscess cavity 
containing 2 oz. of grumous fluid. Both kidneys were much enlarged, 
each weighing over 9 oz., fatty and congested ; the left contained 
an abscess on its cortical surface, closely connected with the penne- 
phritic fat. The liver was of great size, weighed 71 oz., was very 
fatty and congested, the gall-bladder was distended with numerous 
faceted calculi, sixty-six in number, and in the aggregate weighing 
106 grains. These were of about equal size, yellow colour, and com- 
posed largely of cholesterin. The majority presented an appearance 
that is usually attributed to spontaneous fracture during life ; one 
side of the stone exhibits the internal structure, but the surface is 
smooth and glistening, and the edges are worn and rounded off. 

The man had always been exceedingly stout, and for some time 
had suffered from a large fatty heart, with valvular incompetence. 
In 1895 he had an attack of gout. A month before he died he had 
hepatic colic with jaundice. There was already albumen in his 
urine. Bronchitis set in and general anasarca followed. 

January 17^^,1899. 


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47. Sarcoma of pancreas ; glycosuria. (Card specimen.) 

By T. Chttbton, M.D. 

RB — , a coal miner aged 54, height 5 feet 5 inches, weight 
• 8 St. 4 lbs., formerlj 10 st. 2 lbs., was admitted into the Leeds 
Infirmary on March 12th, 1898, for pain in left side of chest or 
npper part of abdomen. Muscles and adipose tissue wasted. There 
were no teeth in the upper jaw ; no complaint of dyspepsia ; recent 
constipation. Urine 38 ounces daily; sp. gr. 1035, sugar, no 
albumen. Badials rather thick. Slight pain in left elbow ; occa- 
sional tingling in right little finger. His mother died young. At 
twenty-seven he had sciatica^ for five months ; at forty-nine, in- 
fluenza; never quite so well since, but was at work and not ill until 
March 10th, 1898 ; on this day he had chills followed by slight 
cough and dyspnoea. 

March 26th. — ^Diabetic diet ordered, in aid of diagnosis. 

April 1st. — ^Diarrhoea; urine 29 ounces, sugar 350 grains, no 

2nd. — Diarrhoea checked by opium and catechu. Temperature 
began to rise. Diabetic diet stopped. 

4th. — Temperature 105'5° at midnight ; urine in previous twenty- 
four hoTU-s 43 ounces. 

5th. — ^Patient died. 

Post-mortem. — The pancreas was not markedly enlarged, but when 
incised its structure appeared almost homogeneous, whitish, and 
not showing the familiar finely lobulated or fissured section-surface. 
Microscopically, the connective tissue was infiltrated with small 
round-cell sarcoma ; the lobules were also invaded, and in some of 
them the normal epithelium was replaced by sarcoma cells ; here 
and there some of these cells had fallen out, leaving small cavities 
whose walls were formed by the growth. In the liver there were 
many spherical and (near the surface) hemispherical growths. 
Simple adhesions had been formed between the pancreas, left 
kidney, and spleen. November Ist, 1898. 

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1. Contracted kidney with multiple adenomata, [Card speci- 

By F. Pabkes Webee, M.D. 

THE kidney is small, hard, and typically " cirrhotic," weighing only 
about li ounces. When first removed from the body it was red, 
and contained a number of small yellowish-white nodules scattered 
over the outer part of the cortex beneath the capsule. These little 
tumours were of rather soft consistence, somewhat resembling 
tuberculous nodules in process of caseation. Microscopical exami- 
nation shows them to be multiple papillary adenomata, such as 
Charles Sabourin ^ described in connection with granular kidneys. 
The structure is that of a cyst filled with delicate branching 
papillary growths, the walls of the cyst and the papillary processes 
being covered with a more or less cubical epithelium. No concen- 
trically marked bodies, such as are termed " corpora amylacea " (or, 
when hard and gritty, " microscopic calculi ") were found in this 
case, though their presence has sometimes been noted in or about 
similar small renal adenomata in other cases.^ 

The present kidney (the right kidney) is from a man aged 57, 
who had a large aneurysm of the transverse part of the arch of 
the aorta pressing on the trachea. 

It may be remarked that no adenomata were observed in the 
man's other kidney (the left one) which was much the largest and 
healthiest of the two. As Sabounn ^ has pointed out, there seems 

* "Sur qnelques cas de cirrhose r^nale avec ad^uomes multiple^,*' * Revue du 
m^deciiie,' PHri^ 1884, p. 441. 

' Sabourin, loc. cit., p. 446; F. Parkos Weber, 'Trans. Path. Soc. Lond.,* 
vol. xlix, p. 177. 

> Sabourin, loc. cit. 

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to be a special connection between these multiple tumours and 
chronic renal fibrosis; this connection is of great interest in the 
question of the general influence of chronic irritation (or chronic 
inflammation) on the development of tumours. Kelynack ^ thinks 
that the adenomata described by Sabourin and Oetlinger, in con- 
nection with interstitial nephritis, are probably more " of the nature 
of a glandular proliferation than true growths."^ The occurrence, 
however, of these little tumours in contracted kidneys reminds me 
of the mtdtiple cutaneous tumours sometimes produced by chronic 
irritation or inflammation of the skin (such as by the chronic action 
of some ejrtemal irritant, as in some trades, or by the prolonged in- 
ternal use of arsenic). Papillary adenomata of contracted kidneys 
probably sometimes develop in connection with the little cysts,^ 
whose presence constitutes a frequent characteristic of chronic inter- 
stitial nephritis. According to my view, such tumours may be 
regarded as analogous to multiple warty growths developing on a 
chronically irritated skin, or to multiple excrescences of the mucous 
membrane occurring in some cases of balanitis, <&c. It seems, 
indeed, as if in certain kidneys, as in certain skins and mucous mem- 
branes, chronic irritation may lead to the formation of multiple 
warty growths, though in many individuals similar irritation does 
not induce a similar development of tumours. 

Jcmuary Srd, 1899. 

1 T. N. Kelynack, * Renal Growths,' Edinburgh and London, 1898, p. 115. 

* In this connection R. Marie's observation is very interesting. This experi- 
menter (* Proceedings of the Auatoinical Society of Paris,* January 27th, 1899), 
in the case of twenty -five dogs, grafted a fragment of renal cortex below the 
capsule of the kidney. In two of these cases a small tumour developed from 
the graft, having somewhat the appearance of an alveolar renal adenoma. The 
growth was destitute of glomeruli, and consisted of acini without any central 

' Papillary adenomata of the kidney easily undergo degenerative changes. 
It is probable that their growth and subsequent degeneration give rise to the 
formation of small cysts in the renal cortex filled with a pultaceous dShrit, In 
the contents of this kind of cyst I have several times recognised the presence of 
minute concentrically marked spherules (" corpora amylacea '* or " microscopic 
calculi "), such as are also seen in sections of renal adenomata. 

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2, Small true lipoma of kidney, (Card specimen,) 
By F. Pabkes Wbbee, M.D. 

THE little tumour, of the size of a millet seed, is situated in the 
renal cortex close to the capsule. It is made up of ordinary 
fat cells of various sizes closely packed together, mostly without 
any fibrous tissue intervening. Here and there, however, especially 
around one or two relatively large blood-vessels, are collections of 
fibroid cells, some of which contain small fat globules. These cells 
are, doubtless, those from which the ordinary fat cells of the tumour 
are formed. There is no distinct capsule, and the little tumour 
has therefore a slightly irregular margin. A study of the micro- 
scopic sections in the present case makes it probable that the tumour 
has originated from a focal multiplication of peri-vascular and 
intertubular fibroid cells, which, after multiplication, undergo fatty 
metamorphosis, and produce atrophy of the glandular cells they 
press on. 

Virchow * speaks of fatty nodules sometimes found in the renal 
cortex, which may attain the size of a cherry. He mentions these 
as examples of heteroplastic lipomata, ihere being no true fatty 
tissue normally present in the kidney substance. 

Dr. T. N. Kelynack^ says, "True lipomata are extremely rare. 
Small aggregations of fat, however, are sometimes found in a 
subcapsular position." Though some of the so-called lipomata 
alluded to by Robin and Virchow have, as Kelynack states, been 
shown by P. Grawitz ^ and others to be small adenomata, arising 
from aberrant adrenal tissue; the occasional occurrence in the 
kidney of small genuine lipomata has been admitted by Grawitz 
himself (in 1884),-* Rudolf Beneke,^ and others.^ Virchow 7 had 

> * Die kraukhaften Geschwaiste,' Berlin, 1863, vol. i, p. 885. 
3 ' Renal Growths,' Edinbnr^h and TiOndon, 1898, p. 62. 
' ** Die togenannten Li pome der Niere," * Virchow's Arch.,' 1888, vol. xciii, 
p 39. 

* Referred to by Aliberg, * Arch. f. klin. Chirurgie,' Berlin, 1892, vol. xHv, 
p. 461. 

* 'Ziegler's Beitrilge zur path. Anat^' Jena, 1891, vol. ix, p. 475. 

* Referred to by AUberg, loc. cit. 

' Referred to by Warthin, * Journal of Pathology,' 1897, vol. iv, p. 410. 

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himself seen but one renal lipoma, wliich he explained as originating 
from a fibroma, the connective-tissue cells of the tumour becoming 
transformed into fat cells. 

Dr. A. Alsberg^ some years ago removed an enlarged right 
kidney from a woman aged 40, supposing it to be the site of 
malignant disease. The kidney was found to contain a large 
number of encapsuled lipomata or fibro-lipomata, varying from the 
size of a millet seed to that of a walnut. They were tolerably 
uniformly scattered through the substance of the kidney, some 
below the capsule, some near the hilum. Some of the tumoiu*s 
were pure lipomata, some contained a good deal of connective 
tissue. In the very vascular young fibroid tissue found near the 
lipomatous nodules the microscope revealed the presence of scattered 
fat cells, and in some parts there were so many fat cells seen, that 
it seemed as if the fibroid tissue was becoming transformed into 
fatty tissue. 

A large single genuine fibro-lipoma, growing from the left kidney 
of a woman aged 31, has quite recently been described by "Dr. A. S. 
Warthin.* It weighed two pounds, and was successfully removed 
during life, being perhaps the only instance, excepting Alsberg's 
case, of surgical interference being required on account of renal 

The renal lipoma in the present case was from a man aged 70, 
with granular kidneys, who died in an apoplectiform condition at 
the Carman Hospital. At the necropsy some minute nodules and 
small whitish spots were seen in the renal cortex below the capsule. 
The small lipoma was one of them. Another of them was apparently 
merely a minute cyst with inspissated contents.^ From naked-eye 
examination I supposed the kidneys contained multiple papillary 
adenomata, which not very rarely develop in cases of chronic inter- 
stitial nephritis, and the present case serves to illustrate the fact 
that various minute tumours (fibromata, lipomata) of the renal 
cortex may easily be set down as adenomata if no microscopic 
examination be made. 

1 "Ueber einen Fall von Lipom der Niere/' ' Arch. f. klin. Chirargie/ Berlin, 
1892, vol. xliv, p. 458. 

> "Fibro-lipoma of the Kidney," ' Journal of PHthology,' Edinburgh and 
London, 1897, vol. iv, p. 404. 

' For the microscopic sections I have to thank Dr. Krieg, one of the resident 
medical officers at the German Hospital. 

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The present case shows, 1 think, how genuine ("heteroplastic") 
lipomata may develop in the kidney substance by the multiplication 
of fibrous or young connective-tissue cells (probably chiefly those 
connected witJi the outer walls of blood-vessels), and the subsequent 
metamorphosis of these newly-formed cells into ordinary fat cells. 
The present case therefore confirms the views of Virchow, Beneke, 
Alsberg, and Warthin as to the origin of renal lipomata by the 
fatty transformation of proliferating fibroblastic cells, or of older 
connective-tissue cells. March 2l8t, 1899. 

3. An undescended left testicle. 
By Abthub Voblckbb, M.D. 

THE left testicle is seen lying in the peritoneal cavity and adherent 
to the posterior layer of the parietal peritoneum. The right 
testicle occupied its normal position. 

From a man aged 32, who had spina bifida and talipes equino- 
varus, and had never walked. He developed an epitheliomatous 
new growth either at the anus or at the seat of a perinseal sinus. 

Decemher 7th, 1898. 

4. Prostatic myornata and vesical calculus removed from the 
same patient. {Card specimen,) 

By T. Cabwabdinb, M.S. 

THE patient was a melancholic individual, 64 years of age, who had 
suffered from retention and from profuse heematuria with but 
little pain. The vesical sound, passed to the hilt, detected a rough 
calculus in the right retro-prostatic pouch. Supra-pubic cystotomy 
was performed and an oxalate and phosphate calculus removed. A 
large soft prostate was felt to project into and occupy almost the 

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whole of the contracted bladder, and corresponding to it in form. 
A week afterwards, before the wound had closed, the prostate was 
incised and several spheroidal masses enucleated with the finger. 
They were about eight in number, varying from the size of a 
pigeon's egg to that of a hazel nut, and after their removal there 
appeared to be a direct channel from the bladder into the urethra. 
The patient got up three weeks afterwards, but eventually ursemia 
supervened. At the autopsy the ureters were foimd enormously 
dilated and the kidneys hydronephrotic. 

January I7th, 1899. 

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Plate V, 

Illustrating Mr, S. G. Shattock's paper upon an Acromegalic 
Skull and that of a normal giant. (Page 185.) 

Fig. 1.— a front view of tbe skull of the normal giant described, showing 
the absence of increase in the height of the superior maxillsD, so notable in the 
acromegalic skull. 

Fig. 2. — A lateral view of the same skull. 

(Photographed by permission of the Council of the Royal College of 

Plate VI, 

Fig. 1. — A front view of the skull described, showing its massive character, 
the notable increase in height of the upper jaw and width of the lower jaw 
between the angles. 

Fig. 2.~A lateral view of the same skull, showing the elongation of the lower 
jaw, leading to notable prominence of the chin, and the increased height of the 

(Photographed by permission of the Council of the Royal College of 

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Path. Soc. Trans. Vol. L. Pl. V. 

Fig. 2. 

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Fig 2. 

Path. Soc. Trans. Vol. L. Pl. VI. 

Fig. 2. 

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1. An acromegalic skull and that of a normal giant. 

By Samuel Q-. Shattock. 

[With Plates V and VI.] 

THE first of these two skulls is from the collection of modem 
Italian crania, purchased by the Royal College of Surgeons in 
1870 from Dr. Giustiniano Nicolucci. Though placed by Sir 
William Flower amongst the normal European crania, it was noted, 
at the time when catalogued, as " of great size, massive and rugged." 
There is no difficulty in recognising it now as one of the acromegalic 
type. I have thus described it in the Pathological Catalogue, to which 
part of the collection the specimen has been recently transferred. 

The skull is unusually massive in consequence of a difhise 
thickening which involves the frontal, the parietal, and all the 
bones and portions of bones entering into the formation of the roof 
and sides of the cranial cavity; below the level of the superior 
curved line, however, the occipital bone is not thicker than natural. 
Similar changes are recognisable in the malar bones, the zygomatic 
processes of the temporals, the palatine processes, and adjoining 
parts of the superior maxillae. The thickened bones are dense, and 
for the most part unnaturally porous and slightly roughened, the 
surface changes being less marked over the area corresponding 
with the origin of the temporal muscle. The pituitary fossa is 
considerably enlarged, indicating the existence of a pituitary goitre. 
The posterior part of the interparietal suture is obliterated. None 
of the foramina at the base are diminished in size. The lower jaw 
is markedly enlarged, but without such thickening as could be 
called massive. The length of the vertical ramus is increased, the 

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chin pointed and unusually prominent. The general enlargement 
is evident, however, in the divergence of the posterior margins of 
the vertical rami, and in the increase in the lower dental arch, which 
everywhere exceeds the upper. Although the circumference of the 
skull is 570 cm., its capacity is but 1500 c.c. 

The parietal bones, where thickest, viz. in the neighbourhood of 
the interparietal suture, measure 2 cm. (^ inch), and in section 
they are closely cancellous or compact, without distinction of tables 
and diploe. The vascular grooves on the inner surface of the skull 
are deepened, showing that the bone has been thickened from 
within as well as from without. 

The texture on section is indistinguishable from that of a calvaria 
thickened and sclerosed in the later stages of osteitis deformans. 

Although Marie's differentiation of acromegaly is so comparatively 
recent as 1886, examples of the condition itself have been put on 
record at earlier periods ; the history of the disease, in this respect, 
running somewhat parallel with that of osteitis deformans, which 
had been nine years previously differentiated by Sir James Paget. 

The earliest apparent example of acromegaly recorded in this 
country is to be found in the Society's 'Transactions,* vol. viii, 
1857, under the title of " Partial Dislocation of the Lower Jaw from 
an Enlarged Tongue,'' by Mr. W. 0. Chalk. This has been referred 
to by various writers upon acromegaly. 

In this case the projection of the lower jaw was very conspicuous, 
and amongst the details in the long but diffuse history given, it is 
stated that at the age of thirty the surface of the body became 
greatly swollen, the swelling, however, being eventually confined 
chiefly to the hands and face ; it was at this period that the tongue 
began to enlarge, and in twelve months afterwards an altered 
condition of the lower jaw was first observed. The ultimate history 
of the case is unknown. The enlargement of the jaw serves here to 
differentiate the condition from that of myxoedema, where the tongue 
may equally be enlarged. 

In 1879 Professor D. J. Cunningham, ( ' Journal of Anatomy 
and Physiology,' vol. ix ) described an example of " A large Sub- 
arachnoid Cyst" from a man suffering from diabetes mellitus; "a 
man of huge frame, with an impleasing expression and overhanging 
brows; his hands and feet were enormously large and flat, and 
his movements clumsy and ungainly." The enlargement of the 
pituitary body and of the pituitary fossa was noticed by Professor 

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Cunninghani, who compared the case with that recorded by Henrot 
in 1877 ( ' Union M^cale et Scientifique du Nord-Est ' ). 

The skeleton of this subject was afterwards described with great 
detail by Br. Alexis Thomson as one of acromegaly ( * Journal of 
Anatomy/ vol. xxiv, p. 488). Of the cranial bones in this instance, 
Dr. Thomson remarks that, as seen in the section by which the cal- 
varia was removed (at the level of the summit of the frontal sinuses), 
they show alterations which are of the nature of an hypertrophy of 
their normal structure, viz. an external and an internal plate of 
compact bone with intervening diploe, increased in thickness and in 
density. " Herein," he proceeds, " lies the difference between the 
hypertrophied bone of acrom^^aly and the diseased bone of osteitis 
deformans ; for in the latter the outer table becomes porous and 
spongy as a result of inflammatory changes, and the normal 
distinction between the outer and inner tables and diploe is lost." 
This generalisation the specimen under consideration shows to be 

In the case, moreover, recorded by Mr. Percy Furnivall in the 
Society's 'Transactions' of last year (p. 207), the skull-cap was 
** thick, dense, and heavy .... there is no distinction between the 
compact and cancellous tissue of the bones forming the skull- 
cap." We cannot, therefore, name these changes hypertrophic in 
the strict or academic sense. They are not such as are seen in the 
form of thickening which is adduced by Sir James Paget as typical 
of true osseous hypertrophy,^ and as arising in connection with 
atrophy and shrinkage of the brain. I have myself seen one 
instance in which such true hypertrophy was limited to one side of 
the calvaria, the change being associated with general atrophy of 
the corresponding cerebral hemisphere. Portions of the calvaria 
from this case are preserved in the museums of University College 
and St. Thomas's Hospitals (No. 342). The subject was a man who 
had suffered when young from epilepsy, and who became afterwards 
a criminal lunatic. 

There is an admirable figure of precisely the same one-sided 
hypertrophy of calvaria associated with hemiatrophy of the cere- 
brum in Cruveilhier's 'Anatomie Pathologique,' planche v, viii^ 
livraison. There was in this case excess of fluid beneath the 
arachnoid, combined with internal hydrocephalus on the atrophied 
side. The author remarks that the fliiid in both positions appeared 
* • Surgical Pathologj,' 3rd edit., p. 60. 

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to be a result and not the cause of the atrophy, and asks whether 
the calyarial thickening was not likewise a result, obserring that 
this could not be the cause, since the cerebral atrophy was not pro- 
portionate to but exceeded it. 

Cruveilhier appears to have been the first to point out the 
sequence between the two events, Dr. Sims's paper upon this subject 
having been published in the nineteenth volume of the * Transac- 
tions ' of the Eoyal Medical and Chirurgical Society, May 26th and 
June 9th, 1836, at which date the particular part of the * Anatomie 
Pathologique ' relating to this subject was already extant. 

One of Dr. Sims*s conclusions is that ** in cases of atrophy of 
the brain the place previously occupied by cerebral substance is 
supplied by serous fluid or by deposition of bone, and this deposit 
of bone frequently takes place on the inner surface of the cranium." 
Another example is that in Van der Kolk's " Case of Atrophy of the 
Left Hemisphere of the Brain with co-existent Atrophy of the Bight 
Side of the Body " (The New Sydenham Society's translation by 
"W. D. Moore, 1861, vol. ii). This writer also observes that in 
unilateral atrophy of the brain there may be either an associated 
corresponding hypertrophy of the calvaria, or that the atrophied 
side may be filled with serum without the bone being thickened. 

Sir George Humphry has discussed the explanation of such 
osseous overgrowth with his peculiar skill in a paper in the * Medico- 
Chirurgical Transactions,' vol. Ixxiii, p. 327. Both the serous 
effusion into the meshes of the pia mater and the thickening of the 
skull attending shrinkage of the brain, proceed, he remarks, from 
a dilatation of vessels consequent upon the diminished volume of 
the cranial contents, and a slowing of the circulation through the 
dilated vessels ; and he aptly compares the condition with that of 
the parts beneath a cupping-glass or other exhausted receiver. 

The following measurements of the acromegalic skull under con- 
sideration were made by Sir William Flower, and are those which 
are systematically carried out upon the crania comprising the 
extensive collection the College possesses : 

C. 525 millimetres. B. 156 millimetres. 

L. 198 „ H. 130 

B.i. 788 „ H.i. 657 

B.N. 104 „ B.A. 102 

A.i. 981 „ N.h. 61 

N.w. 25 „ N.i. 410 

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O.w. 44s millimetres. O.h. 41 millimetres. 

O.i. 932 „ C.a. 1500 com. 

C. Horizontal circumference taken with the tape passing in front 
round the supra-orbital line (above the glabella), and behind across 
the most prominent part of the occiput. 

L. Length. Taken from the ophry on or centre of the supra-orbital 
line above the glabella to the most distant part of the occiput. 

B. Breadth. The gi'eatest parietal breadth. 

Bi. Index of length, 1_2LJ:22- 


H. Height. The distance between the basion (middle of the 

anterior margin of the foramen magnum) to the bregma (point of 

junction of the coronal and sagittal sutures). 

Hi. Index of length, ?- A_i^- 


BN. Basi-nasal length. Basion to nasion (middle of the anterior 
margin of the foramen magnum to middle of the naso-frontal 
suture at the root of the nose). 

BA. Basi-alveolar length (basion to alveolar point or the most 
distant part of the anterior margin of the alveolar arch). 

Ai. Alveolar index, -^4 >< iP9- 

Nh. Nasal height (the distance between the nasion and lower 

border of the nasal aperture). 

Nw. The greatest width of the nasal aperture. 

XT- XT 1 • - Nw. X 100 

Ni. Nasal maex, -, • 


Ow. Orbital width. From the spot where the ridge which forms 
the posterior boundary of the lachrymal groove meets the fronto- 
lachrymal suture, to the most distant part on the front edge of the 
outer border of the orbit. 

Oh. Orbital height. The distance between the upper and lower 
margins of the orbit at the middle. 

Oi. Orbital index. Oh^iLJOO- 

Ca. Capacity in cubic centimetres. 

In the acromegalic type of cranium, however, the elongation of 
the superior maxillae and increased volume of the lower jaw 
constitute the salient feattu^s ; and as these are not indicated by 

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the foregoing measurements (with the exception of the nasal 
height or distance between the fronto-nasal suture and lower 
border of the nasal aperture), I may add to Sir William Flower's 
table those particularly relating to the jaws, adopting for this 
purpose Sir William Turner's scheme of mensuration ("'Chal- 
lenger' Eeport on Human Crania," *Zool. Chall. Exp.,' vol. x, 
1884), especially as this has been employed by Dr. Alexis Thomson 
in the case already adverted to. The particular craniometer used 
was that devised by Sir William Flower, and described by him in 
the Anthropological Catalogue of the College. 

Naso-alveolar height. — From the nasion or middle of the naso- 
frontal suture at the root of the nose to the alveolar point or 
centre of the anterior margin of the upper alveolar arch, 88 
millimetres. (In Dr. Alexis Thomson's acromegalic skull this 
measurement is 81 millimetres.) 

Nasal height. — Between nasion and lower border of the nasal 
aperture, 61 millimetres. (In Dr. Thomson's skull, 59 milli- 

Facial length. — Vertical diameter of the face from the nasion to 
the lowest point in the mid-line of the lower jaw, 143 millimetres. 
(In Dr. Thomson's skull this is 148 millimetres ; and he adds that 
he f oxmd the average in ten adult Scottish crania in Sir William 
Turner's collection to be 124*5 millimetres.) 

Taking next the measurements of the lower jaw. As in other 
typical examples of acromegaly, the mandible is abnormally 
prominent at the symphysis. 

Symphysial height. — Extreme vertical measurement at the sym- 
physis, 40 millimetres. 

Condyloid height. — Distance from the angle or gonion to the 
upper surface of the condyle, 93 millimetres. (In Dr. Thomson's 
skull this is 90 millimetres.) 

Breadth of ascending ramus. — At the level of the alveolar 
border, 38 millimetres. (In Dr. Thomson's skull this is 36 

Intergonial width. — Extreme width between the angles. 111 
millimetres. (In Dr. Thomson's skull this is 101 millimetres.) 

Dimensions of the enlarged pituitary fossa. — Antero-posterior 
diameter, 20 millimetres. Transverse diameter, 20 millimetres. 
Depth, 20 millimetres. (In Dr. Thomson's skull the correspond- 
ing diameters are 22*5, 21, 18 millimetres.) 

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The relation of acromegaly to giant growth has been variously 
stated. Some have maintained that when the disease arises in 
youth, giant growth results; when in the adult, it assumes the 
form of simple acromegaly ; and further, that all giants are acro- 

In the College Museum there are the skeletons of two giants 
(Nos. 223, 224). That of Charles Byrne or "O'Brian" (7 feet 7 
inches) I should view, with Dr. D. J. Cunningham (* Transactions 
of the Royal Irish Academy,' 1891), as acromegalic. The lower jaw 
is massive, the chin particularly prominent, the glabella veiy pro- 
jecting, and the cranial bones dense and thickened ; the pituitary 
fossa measures antero-posteriorly 22 mm. The capacity of this 
skull is 1520 c.c. ; its circumference, 1500 mm. Byrne died at 
the age of 22. Neither his father, mother, brother, nor any other 
member of his family was of unusual size. Though commonly 
known in London &s the Irish giant, this skeleton is not to be 
confounded with that of Cornelius Magratb, in the Museum of 
Trinity College, Dublin, which is fully described by Dr. Cunning- 
ham (loc. cit.), who showed it to be that of an acromegalic, the 
pituitary fossa being considerably enlarged and its boundaries 

The Irish giant referred to in Sternberg's monograph is the 
one in Dublin, Byrne having escaped that author's notice, probably 
owing to the source of confusion pointed out. 

The other giant skeleton in the College collection is 6 feet 8 
inches in height (2030 mm.), and is that of a man known as 
Freeman, the American giant, who died in 184?5 in the County 
Hospital, Winchester, having come to London in 1842 and trained 
for a prize fight. In the College catalogue he is erroneously stated 
to have died in 1854. This man was known to and examined by 
Mr. J. Hutchinson, who has given his respiratory capacity in 
his classical paper "On the Capacity of the Lungs," 'Medico- 
Chirurgical Transactions,' vol. xxix (1846). Freeman's death took 
place from phthisis ; this was indicated during life by the expecto- 
ration of large quantities of pus and extreme emaciation. After 
death extensive tuberculosis of the lungs was found. In regard 
to this skeleton I have come to the conclusion that it is not one 
of an acromegalic but of a normal giant; and for this reason I 
append photographs of the skull, together with a series of mea- 
surements corresponding with those given under the acromegalic 

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specimen. The exterior of this skull is everywhere smooth, nor 
is there anywhere anything suggestive of abnormality in the osseous 
tissue. The thickness of the calvaria at a distance of 20 mm. 
behind the bregma does not exceed 6 mm., and the trephined 
surface displays a normal distinction of tables and diploe. A 
certain degree of prognathism is present, but in itself this is not, 
of course, a pathological feature. I have given its actual degree 
further on. The most remarkable difference between this skull 
and the acromegalic is brought out by the altitudinal measure- 
ments of the upper and low^r jaws. 

The naso-alveolar height is but 76 mm., as contrasted with 88 
mm. ; the nasal height is 50, as contrasted with 61 ; the condyloid 
height of the lower jaw is but 73, as contrasted with 93 in the 

The following are the measurements of Freeman's skull deter- 
mined by Sir William Flower : 
C, circumference, 540 mm. 
L., length, 191. 
B., breadth, 145. 
B. i., index of length, 759. 
H., height, 149. 
H. i., index of height, 780. 
Capacity, 1630 

To these I may add the following from my own determina- 
tions : 

Pituitary fossa ; antero-posterior diameter 12 mm. 

Naso-alveolar height 76, 

Nasal height 50. 

Facial length 134. 

Symphysial height of lower jaw 37. 

Condyloid height 73. 

Breadth of the ascending ramus 40. 

Intergonial width 101. 

Alveolar index 1026. 

Although Sir William Flower gives (in his preface to the College 

Anthropological Catalogue) as the formula for determining this 

B a X 100 
index — ^^1^= » all the alveolar indices in the catalogue have 

been taken by multiplying with 1000 instead of 100. By this 

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means a result is obtained in three or four figures, which dispenses 
with the use of decimals or fractions. 

BaxlOOO 117x1000 -^^^ 
B N = ^114^' - ^^^^ 
The alveolar index, as a measure of prognathism, was introduced 
by Sir William Flower, and it is one of the least open to objection, 
giving, as it does, the relation of the two distances : (1) from the 
anterior margin of the foramen magnum to the root of the nose ; 
(2) from the anterior margin of the foramen magnum to the most 
projecting point of the upper jaw. 

Sir William Flower has divided crania, according to their alveolar 
indices, into— 

Orthognathous ; index below 980. 

Mesognathous ; index 980 to 1030. 

Prognathous ; index above 1030. 

Freeman's skull, therefore, with an index of 1026, stands below 
the prognathous series of this scheme. 

The European and English skulls in the college collection come, 
as a whole, within the orthognathous division. 

Nothing being known of Freeman's ancestry, it is impossible to 
say whether or not the mesognathism indicates a racial mixture. 

The American Indians of all tribes in the college collection, 109 
in number, give an average alveolar index of 1020 ; they are 

The prognathism of the African negroes (who present this 
feature in the highest degree) is 1044. 

Individuals in all races may considerably exceed the average 
Among the Australian skulls (which are prognathous) is one with 
an alveolar index of 1071 ; another reaches the extreme of 1083. 
Of the European skulls Sir William Flower determined, moreover, 
that 734 per cent, were orthognathous; 201 mesognathous; 6*5 

In his 'Elements d' Anthropologic generale* (Paris, 1885), 
Topinard divides prognathism into three kinds, the most important 
of which concerns the alveolar portion of the superior maxilla — 
alveolar prognathism, or the forward projection of the upper jaw 
below the lower level of the nose. In Topinard' s method of 
estimating prognathism the cranium is placed horizontally, resting 
upon the condyles and alveolar point, not the teeth ; a perpendicular 


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is dropped to this horizontal plane, at the alveolar point, and from 
this perpendicular horizontal measurements are taken : (1) to the 
"spinal point" (the lower border of the anterior nares at the 
virtual centre of the nasal spine) ; (2) to the nasion ; (3) to the 
ophryon. Indices may be obtained by taking the height of these 
points and calculating the relation of the horizontal measurements 
to the perpendicular ones ; or the result may be expressed as an 
angle giving the inclination on the horizontal plane of lines drawn 
to the alveolar point from the facial extremities of the horizontals 

In Freeman's skull the horizontal projection of the alveolar 
margin beyond the lower limit of the nose, as measured from the 
base of the nasal spine, is 15 mm., and the height of this horizontal 
above that of the base of the skull on the alveolo-condylar plane is 
25 mm. (alveolar prognathism of Topinard). 

The distance from the perpendicular to the nasion is 24 mm.» 
and the height of this horizontal from the alveolo-condylar plane^ 
74 mm. (maxillary prognathism of Topinard). 

The distance from the perpendicular to the ophryon is 28 mm. ; 
the height of this horizontal from the alveolo-condylar plane is 
101 mm. (facial prognathism of Topinard). 

Topinard's indices are obtained by multiplying the horizontal 
distances by 100 and dividing the result by the vertical. 

Vertical. Horizontnl, Index. 

Alveolar prognathism . . 25 mm. ... 15 unn. ... GO 
Maxillary prognathism . . 74 „ ... 24 „ ... 32'4 

Facial prognathism . . 101 „ ... 28 ,, ... 27*7 

This gives a remarkably high degree of "alveolar prognathism,'* 
and I cannot but feel myself that Sir William Flower's alveolar 
index conveys a more correct idea of the prognathism present in 
the skxdl under consideration than Topinard's. The objection 
thought so weighty by the latter author to Ilower's index — ^viz. 
that it is open to vitiation arising from flattening of the cranial 
base, remains unremoved in the system devised by himseK. In 
Topinard's method the cardinal horizontal plane is obtained by 
resting the skull upon the condyles and alveolar point; and a 
flattened base, by virtually lowering the posterior part of the skull, 
would remove the facial extremities of the three horizontals (to the 

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nasal point, the nasion, and ophryon) away from the perpendicular 
dropped to the alveolar point, with the result of increasing the 
whole of the indices. 

The teeth in Freeman's skull are remarkably perfect, and it is to 
be particularly noted that although " mesognathous," there is no 
projection of the lower jaw beyond the upper The skull in 
acromegaly, on the contrary, is " underhung ; " the lower alveolar 
arch lies without the upper. As Maximilian Sternberg points out, 
this condition is not to be confused with prognathism ; it should be 
distinguished by some special term, such as L. Mayer's, — cranium 
progeneum (progeneus, modem Latin transcript of irpoyerciot). 

Freeman's skxdl is prognathous, not progeneic; and although 
that of a giant it is not acromegalic. According to the computa- 
tion of Sternberg, nevertheless (* Specielle Pathologic und Therapie,' 
Theil 2, Band vii, "Die Akromegalie"), 40 per cent, of giants are 
acromegalic. There are, in short, normal giants and pathological 
giants, as there are normal and pathological dwarfs; and the 
college skeletons of Freeman and Byrne afford examples of each. 

October ISih, 1898. 

2. Symmetrical senile atrophy of parietal bones, {Card 

By H. MoELBY Fletcher, M.D. 

THIS condition of the skull-cap of a woman aged 79, who ^^ .^^^ 
St. Bartholomew's Hospital in consequence of a fractti 
femur, was first discovered at the post-mortem examination. ,*,xx^ 

The Bkull-cap showed a symmetrical thinning of the medial -^^rx^ 
posterior portions of both parietal bones, the osseous tissue ^^^^^-^^rr 
Taeen reduced to a thin transparent sheet of bone, little ^^L^^^xxe 
than ordinary letter paper. There was no thickening of tKe ^^^ ^^ 
at the edges of the thinned area, though there was some ^^^^^.^Xclx 
porosity. The rest of the skull-cap appeared normal. The ^^^j^.g^^jijo. 
grooTes on the inner surface were deeply marked. The 

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beneath the thinned areas and the soft tissues above appeared to 
be normal.i 

Similar cases have been described in these * Transactions ' by Mr. 
F. S. Eve,2 and elsewhere by Sir G. Humphry.^ 

ApHl ISth, 1899. 

3. Crushed fracture of cervical spine. 
By H. P. PoTTEE, M.D. 

THE man from whom this specimen was removed was 82 years of 
age. In 1879, twenty years ago, he was struck on the occiput 
by a falling wall and the cervical spine was forcibly flexed. He 
remained unconscious for two days, but indistinctly remembei*ed 
some one pulling upon his head and twisting it from side to side. 
When consciousness returned he noticed loss of power of the right 
arm and leg, which was only temporary. An immoveable apparatus 
was applied to the head and neck, and he was kept in bed for four 
months ; made a satisfactory recovery and lived till August, 1898. 

When I first saw the man in 1880, there was a hard prominence 
in the median line at the back of the neck, extending from one inch 
below the external occipital protuberance to the sixth cervical 
spinous process, measuring four inches in diameter. The trapezii 
appeared to be incorporated with the prominence on each side. 
The manubrium stemi, upper three costal cartilages, and larynx 
were abnormally prominent, the chin almost touched the sternum, 
and the posterior boundary of the pharynx could hardly be reached 
with the tip of the finger. Without the history of injury, the 
swelling presented a nice case for diagnosis. 

The specimen is a vertical antero-posterior section through the 
cervical spine and cord. Some crushing force has pressed the 
vertebral bodies into a mass. The intervertebral cartilages have 
disappeared, but their outlines are still marked and their places 

^ The skatl-cap is in St. Bartholomew's Hospital Museam, No. 7a. 

a Eve, • Trans. Path. Soc.,* vol. xli, 1890, p. 242. 

' Humphry, * Trans. Uoy. Med. and Chir. So?.,' vol. Ixxiii, 1890, p. 327. 

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are occupied by bone. The axis or second vertebra is at right 
angles to the spine ; the third body is much deformed, the fourth 

Fig. 17. 

is a six-sided figure in the section, the fifth has become a perfect 
triangle ; the sixth and seventh are displaced and pressed together, 
so that the distance between the upper extremity of the axis and 
the lower border of the seventh cervical is reduced to two inches. 
The spinal cord is probably not stretched, although it is bent 
round the prominence of the bodies, nor is the spinal canal 
encroached upon by displaced vertebrse. There has probably been 
hsemorrhage external to the sheath, for suggestive organised shreds 
still remain. 

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The conditions shown in the specimen are somewhat tmusnal, and 
I have not been able to find a preparation in the London museums 
of a similar nature. Great force must have been applied to the 
spine, but the direction of this force was fortunately such that 
dislocation and sudden death did not ensue. On the other hand, 
the man, as I have stated, lived twenty years after the injury, and 
finally died from senile decay. January nth, 1899. 

4. Ctnirai sarcoma of os calcis, {Card specimen,) 
By P. DE Santi. 

PATIENT aged 22, an out-patient at Westminster Hospital, com- 
plained of pain and swelling in outer part of os calcis, and on 
walking had a sharp shooting sensation in the foot. No history 
of injury was obtained. He had noticed the swelling about six 
months. On examination a tender, ill-defined swelling was found 
over the outer part of os calcis, with some redness of skin and 
oedema. There was no synovitis of the ankle-joint. There was no 
history of tubercle or syphilis. No wasting or trouble elsewhere. 

An exploratoiy incision was made, the case being regarded as pro- 
bably one of tubercle of the os calcis. The swelling turned out to be a 
spindle-celled endosteal sarcoma infiltrating the surrounding tissues 
and completely filling the os calcis. The leg was removed just 
below the knee-joint, and the patient made an excellent recovery. 
The interest of the case consisted in the diagnosis between tubercle 
and sarcoma - the i>ain and tenderness on pressure, the redness, 
oedema, and absence of any egg-shell crackling pointed to tubercle 
or chronic abscess of bone. The history of no injury and six months 
duration were in favour of sarcoma. It was not until an exploratory 
incision was made that an absolute diagnosis could be made. 
Another point of interest was the microscopic appearance of the 
growth ; usually endosteal sarcomata were myeloid, in this case it 
was a spindle-celled sarcoma. January Srd, 1899. 

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5. A case of apparently aseptic suppuration of the knee-joint 
following injury, and associated with phagocytosis of ex- 
travasated red blood- corpuscles by leucocytes. 

By F. W. Andeewbs, M.D. 

NON-BACTEBiAX suppuration is well known as an experimental 
fact, but is mncli rarer clinicallj. The present case is brought 
forward as an example of well-marked acute suppurative arthritis 
coming on a week after injury, in which no micro-organisms were 
demonstrable either microscopically or by culture on repeated exami- 
nation, but in which blood appeared to have been originally effused 
into the joint ; the red corpuscles being disposed of by a process of 
phagocytosis during the inflammatory reaction. 

A man aged 25 was injured on April 29th, 1897, by a heavy door 
falling on him and striking him on the right loin. Profuse heema- 
turia followed, apparently due to laceration of the kidney. He was 
admitted to St. Bartholomew's Hospital under Mr. Willett, and the 
hsematuria cleared up in a week or two. There had been some pain 
in the right knee from the time of the accident, but the knee was at 
first to all appearances normal. The pain grew worse, and on May 
6th, a week after the accident, the temperature rose. Next day 
there was a little grating in the joint but no effusion. 

On May 11th the fever varied from 101° to 103°, and there was 
much effusion into the joint, with intense pain and tenderness, but 
no redness. It was decided to aspirate the joint, and this was done 
on four occasions, on May 11th, 13th, 14th, and 15th, each time 
with relief, from 3 to 5 oz. of synovia mingled with blood and 
pus being withdrawn on each occasion. By May 19th the fever 
had disappeared, and there was no longer any effusion into the 
joint. The patient eventually recovered without any appreciable 
loss of mobility of the joint. 

Three of the four specimens of fluid removed from the joint were 
submitted to me for examination, — the first, second, and fourth 
aspirations— two days interval elapsing between each aspiration. 

The fluid from the first aspiration separated on standing into a 
nearly clear viscid synovia, somewhat bloodstained, with an abundant 

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deposit of red blood-corpuscles and pus cells, the latter prepon- 
derating. The pus cells were very large, and contained abundant 
brightly ref ractile fat granules ; nuclei polymorphous and beginning 
to undergo fragmentation. Most of the red corpuscles were free, 
but many were included in the large leucocytes, sometimes two and 
even four in one leucocyte. The appearance was striking and 
unmistakable in the fresh state, and could be demonstrated equally 
well by careful staining. No trace of any micro-organisms could 
be found in the stained specimens, but I made no cultures from 
this specimen. 

Two days later, at the second aspiration, I made agar-agar 
cultivations direct from the aspirating needle at the bedside ; they 
remained sterile, and again no micro-organisms were microscopically 
demonstrable. This time the fluid was clearer, and on standing, 
perfectly clear synovia separated out above. Much less blood was 
present, and the red corpuscles were more often included in leuco- 
cytes than free. The stained specimens shown were prepared from 
this specimen. 

Two days later still, at the fourth aspiration, the fluid was again 
more turbid and blood-stained, and the deposit more closely re- 
sembled ordinary laudable pus. Hardly any included red corpuscles 
were now present. Again no micro-organisms could be demonstrated 
in any way. 

Clinically the case was clearly one of acute arthritis with a 
considerable amount of pus in the joint, and with fever and 
constitutional symptoms running parallel with, and being obviously 
dependent upon, the joint inflammation. Failure to demonstrate 
and cultivate micro-organisms can by no means be held to prove 
their absence, but my experience has been that it is usually easy 
to demonstrate micro-organisms in acute suppurative arthritis. 

I have met with no similar case, and I bring it forward rather 
with the view of eliciting the experience of others than with any 
pretence at offering an explanation myself. But I suggest that as 
the resiilt of the injury blood was effused into the joint, and 
subsequently setting up irritation, was removed by a process of 
clearly demonstrable phagocytosis, the extent and character of 
which seems to point to the red corpuscles as the irritant agencv, 
I am not by any means an upholder of an exclusively phagocytic 
theory of inflammation. Yet it is certain that phagocytosis does 
occur in inflammations of many kinds ; and I put this case forward 

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as one in which the phenomenon was marked, and very easily 

I may mention in conclusion one or two incomplete observations 
which I made on the fluid withdrawn from the joint. The different 
samples being left about in the laboratory for a week or so, showed 
no tendency to putrefaction. Some of the clear synovia, decanted 
without special precautions into sterilised test-tubes and plugged 
with sterile wool, imderwent no change for many weeks, though 
after a month or two slight bacterial growth occurred in most of 
the tubes. Some of the tubes were inoculated with B, anthracis, 
Staphylococcus aureus, Proteus vulgaris, and B, prodigiosus. These 
all showed good growth in a day or two. Hence there was nothing 
actually germicidal in the fluid, though it was evidently a poor 
soil for bacterial growth. Chemically there was a good deal of 
nucleo-proteid in the fluid ; at least, when digested with HOI and 
pepsin, it gave a considerable insoluble precipitate, which dissolved 
in dilute alkali. May 2nd, 1899. 

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1. Hypertrophy of the pituitary body. 

By J. and T. W. P. Lawrence. 

SINCE the publication of the first descriptions of acromegaly by 
Marie in 1886, a considerable number of specimens of enlarged 
pituitary body have been described. Eather more than one half 
of these have been found associated with acromegaly ; whilst the 
remainder (references to which are appended to this paper) include 
various new growths and enlargements, of which hypertrophy 
forms but a small proportion. Two or three cases only of hyper- 
trophy of the gland, apart from acromegaly, have been placed on 
record, excepting those instances of slight increase in size observed 
in such conditions as myxoedema and cretinism. Since, however, 
the terms hypertrophy and adenoma have sometimes been used 
synonymously in their application to the pituitary body, it is 
possible that the rarity of recorded examples of hypertrophy may 
to some extent admit of explanation. The specimen to be described 
is of interest both as an instance of marked hypertrophy of the 
gland not associated with acromegaly, and as presenting with some 
distinctness the characters which distinguish hypertrophy from 

The patient, a railway inspector by occupation, died at the age 
of fifty -two, the post-mortem examination disclosing enlargement 
of the pituitary body as the cause of death. Six years before his 
death the patient sought medical advice on account of dimness of 
sight, and at that time the field of vision was, on examination, 
found to be cDutracted externally on both sides. No history of 
syphilis, alcoholism, or excessive smoking was obtainable. A trace 
of albumen was present in the urine, but apart from this and the 
dimness of sight the general health was good. The history of the 
case during the succeeding six years is characterised by alterations 
tiffecting the speech and the gait, and by progressive general 

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weakness of the body, and, towards the end, of the mind also. 
The speech gradnallj became much impaired, slow and drawling in 
character, and the gait somewhat ataxic. The contraction of the 
field of vision steadily increased, imtil ultimately the patient was 
only able to distinguish objects situated directly in front of him. 
The patient was confined to bed during the last twelve months of 
the illness ; and latterly a perforating ulcer developed on each foot, 
and the hair was noticed to have become coarser. There was no 
enlargement of the jaw, hands, or feet. 

At the post-mortem examination, which was restricted to the 
cranial cavity, the bones of the cranium were found to be rather 
thin, and the dura mater was more adherent to them than normal ; 
the frontal sinuses were not obviously enlarged. The pituitary 
fossa was expanded by the enlarged pituitary gland, which was, to 
a great extent, of semi-fluid consistence, and could not be removed 

On examination of the base of the brain, the space bounded 
laterally by the temporal lobes and posteriorly by the pons Varolii 
is found to be occupied by a tumour (Fig. 18) measuring nearly 35 
cm. from before back, and about 2*5 cm. transversely; and the 
greatly thinned optic commissure is stretched over the roimded 
anterior surface of the growth. The tumour is divided by a 
shallow transverse groove into an antero-superior and a postero- 
inferior portion. The anterior portion is hemispherical in shape, 
is quite smooth on the surface, and measures 2 cm. in diameter. 
The posterior and larger portion measures nearly 3 cm. at its 
broadest part, and 2*5 cm. from before back; and its surface is 
rendered irregular by a large fissure leading into a cavity in the 
centre of the tumour, the fissure having been produced at the post- 
mortem examination, when a considerable quantity of semi-fluid 
tumour-substance was lost. The surface of the posterior portion, 
although uneven, is smooth, except at the ragged aperture men- 
tioned ; and the whole tumour is covered by a very delicate fibrous 
layer. The growth can readily be raised from surrounding struc- 
tures, being free from adhesions, and it shows no signs of having 
infiltrated the adjacent tissues. The crura cerebri and the optic 
tracts are pushed aside and compressed by the rounded antero- 
superior portion of the tumour, and the optic commissure is less 
than 1 mm. in thickness. 

A median section of the brain exhibits the exact anatomical 

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Fia. 18. 

Hypertrophy of the pituitary body. 

Fig. 19. 


Median section of hypertrophied pituitary body. 

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relations of the tumour (Fig. 19) ; it will be noted, however, that the 
form and position of the several structures are considerably altered, 
owing to some degree of vertical compression of the brain having 
occurred in the process of hardening. There is present on the 
postero-superior surface of the tumour a small fragment of bone 
(d) from the upper margin of the dorsum sellse ; higher up on the 
same surface the lamina cinerea meets the tumour at the apex of 
the infundibulum (a), and the portion of the tumour which is 
situated between these two points may be taken to represent the 
greatly thickened pedicle, whilst the portion below d represents the 
enlarged and excavated body of the gland. In addition to the 
increase of the pedicle in thickness, an extension of this part of the 
growth has taken place in an upward direction, so that the greatly 
stretched anterior wall of the infundibulum, which lies between the 
point a and the posterior margin of the optic commissure b, is 
closely applied to the upper part of the tumour ; and there is a 
further extension upwards above the optic commissure in the form 
of a small nipple-shaped process (&), which projects into the cavity 
of the third ventricle. 

Fig. 20. 

Microscopic appearances of hjpertrophied pituitary body. 

The tumour is imiform in texture and of soft consistence, and it 
presents the same microscopic structure throughout (Fig. 20). In 
those parts in which degeneration has not occurred it is constituted 
of a stroma of very delicate fibrous trabeculse, which separate large. 

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irregpilar, and intercommunicating spaces filled with epithelial 
cells. The cells are polygonal in shape and have an average . 
diameter of 10 micromiUimetres ; they have large, round or oval, 
and deeply staining nuclei, and they appear to be all of the same 
kind. Towards the surface of the tumour the cell spaces become 
narrower and many of them oval in shape, and they resemble 
more closely the alveoli of the anterior lobe of the normal gland 
than the deeper spaces of the growth do. The outermost spaces 
appear in section as narrow clefts, disposed parallel to the surface, 
in what has previously been mentioned as the fibrous covering of 
the tumour, and they are mostly occupied by a single or double 
layer of cells, though from some of them cells are altogether absent. 
Although the cell spaces thus differ somewhat in form in the 
central and in the peripheral parts of the tumour, a gradual 
transition is traceable from the central parts to the peripheral; 
there is no break in the continuity of the tissue, which is of 
essentially the same structure from the surface to the centre of the 
growth. No cysts appear to be present in the tumour, and there is 
no colloid material in the alveolar spaces. Nothing resembling 
the posterior lobe is discoverable either on macroscopic or micro- 
scopic examination. 

The condition described has been called adenoma by some, 
hypertrophy by others; but that the diagnosis of hypertrophy is 
the correct one in such cases seems to admit of little doubt. The 
several parts of the gland are recognisable, and are seen to be 
affected by a diffuse change — ^the glandular portion of the pedicle 
equally with the anterior lobe of the gland — and no encapsuled or 
circumscribed tumour is present. The clinical history, the absence 
of infiltration, and the microscopic examination exclude the expla- 
nation of the diffuse change as possibly being due to an infiltrating 
growth, and the microscopic structure of the tumour is not opposed 
to the diagnosis of hypertrophy. For although the cell spaces of 
the tumour deviate to some extent from those of the normal gland 
in size and in the number of their contained cells, it is to be 
remembered that such deviations are sometimes met with even in 
true compensatory hypertrophy (as in the thyroid gland after its 
partial ablation), and that where the hypertrophy has a pathological 
rather than a physiological origin (as may be presumed to be the 
case in the present instance) some deviation from the normal 
structure is almost to be expected. 

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Waddell (Jr.), ^** Some Clinical Notes on a Case of Tumour of the Pituitary 

Body," 'Lancet,' 1893, vol. i, p. 921 ; and 2%<wJ«r» ( 7F.).—" Tumour of 

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the Pituitary Body," 'Traus. Path. Soc. Manche§ter/ 1891-2, vol. i, p. 70 

(Hypertrophy ?). 
Whitwell (J, B.).—** Tumour of the Pituitary Body," ' Joum. of Ment. Sci.,' 

1889, vol. XXXV, p. 199 (Myxo-tarcoma). 
WilU (^.).— "Tumour of the Pituitary Body without Acromegaly," 'Brain,' 

1892, vol. XV, p. 466 (Goitre of pituitary body). 
Wolf (jr.). — " Bin Beitnig zur Pathologic der Hypophysis," * Beitr. z. path. 

Anat. u. Allgem. Pathol.,' 1898, vol. xiii, p. 629 (Secondary malignant 

ITckMi.— "Tumour of the Pituitary Body," * Lancet,' 1895, vol. i, p. 993 

Woolcombe {W, X.). — "A Case of Virchow's Psammomn of the Pituitary Body, 

with Remarks as to the Function of that Structure," ' Brit. Med. Joum.,' 

1894, vol. i, p. 1861. 

April Uh, 1899. 

2. Two cases of splenic anamia with internal hemorrhages in 



By Qc, Bebtbam Hunt, M.D. 

"^ASES of enlargement of the spleen with severe ansemia in infants 
who are usually rickety are, of course, common; but it ib 
very doubtful whether such cases should be termed splenic anaemia, 
and it has been doubted whether this disease ever really occurs in 
infants. For this reason the occurrence of marked internal hsemor-^ 
rhi^es is of interest. 

The first case was a child of eight months, one of twins. During 
life the spleen reached below the umbilicus and across the middle 
line Red corpuscles 70 per cent. ; hemoglobin 28 per cent. No 
excess of leucocytes. There were no signs of rickets. During the 
disease, which lasted three and a half months, there was irregular 
fever. Severe diarrhoea was present during the last month of life. 

Fost-mortem, — The spleen was much smaller than during life. 
It meastired 6x3 inches. Weight 7 J oz. Capsule thickened. Sur- 
face granular. On section it appeared too uniform, the normal pulp 
being replaced by a firm, structureless substance. Microscopically 
there was increase of fibrous tissue, not affecting so much the 


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210 DtlCTLlfiSS GLANDS. 

trabeculse^ though these were somewhat thickened^ as the splenic 
pulp, the cells of which were much diminished in number and 
surrounded bj new fibrous tissue. The Malpighian corpuscles 
were almost entirely replaced by freshly formed, structureless 
connective tissue. The mesenteric glands were enlarged aiid of a 
deep red colour. Throughout the whole length of the Jarge gut 
the mucous membrane was thickly studded with small hsemor- 
rhagic patches, varying from one sixteenth to one half inch in 
diameter. Many of these had become ulcerated on the surface, 
and over others there was still an adherent slough. 

Case 2 was a child of sixteen months, one of triplets. It differed 
from the other in presenting marked rickety bone changes. The 
spleen occupied the whole of the left half of the abdomen, reaching 
from the costal margin to the pubes. The liver wa s slightly enlarged. 
Frequent blood estimations gave on an average 30 per cent, of red 
corpuscles and 25 per cent. hsBmoglobin; white to red 1 to 100. 
The red corpuscles were individually of fairly good colour, but 
varied much in shape and size. On staining, some of them were 
seen to be enucleated. There were occasional attacks of diarrhoea, 
and some irregular pyrexia. The child died with severe dyspnoea. 
Post mortem the spleen weighed 4^ ounces, and measured 4^ x 
3 inches. The surface was smooth. Capsule not thickened ; cut 
section dense, pale, and mottled. Microscopically there is se,en the 
same connective-tissue overgrowth in the splenic pulp and fibrosis 
of the Malpighian corpuscles as in the first case. Bones showed 
marked rickets, with red gelatinous marrow. Between the dura and 
arachnoid there was a layer of extravasated blood, in parts one third 
of an inch thick. On the right side it extended from base to vertex, 
and completely covered the cerebral hemisphere; on the left side it 
was less extensive. The blood- clot could be peeled off the dura in the 
form of a thick laminated layer. There were no false membranes 
or other signs of inflammation of the dura. The only symptom 
which could be ascribed to this hsematoma was the terminal 
dyspnoea, which was not accounted for by any pulmonary con- 

The chief point to be considered is whether these are two genuine 
cases of splenic anwmia or not. One great difficulty in dealing 
with these cases in young children is to decide whether they may 
not be simply examples of rickets with anaemia and enlarged spleen. 
There is nothing in the blocd examination which in my opinion is 

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sufficient to distinguish between the ansBmia of rickets and splenic 
an»mia; and, indeed, in the later disease the blood condition is by 
no means constant. The blood in splenic ansemia may on the one 
hand be of the chlorotic type, as described by Banti, and which oc- 
curred in the first of these two cases ; or it may resemble the blood 
of pernicious ansemia, in the great reduction of red corpuscles, 
poikilocytosis, and presence of nucleated red corpuscles. This 
condition of blood was described in cases of splenic anemia by 
Bruhl, and was present in the second of these cases. 

However, I tbiok that rickety aneemia can be satisfactorily ex- 
cluded here. In Case 1 there were no signs of rickets; and in 
Case 2, although there was severe rickets, yet the size of the spleen 
was far greater than that seen in this disease alone. The internal 
haemorrhages, in one case into the mucous membrane of the large 
bowel, and in the other into the cerebral meninges, also form no 
part of rickets. Such visceral haemorrhages have been occasionally 
seen in infantile scurvy, but in the present cases there were 
neither the determining causes nor other signs of scurvy. Lastly, I 
believe that there is considerable difference in the microscopical 
section of the enlarged spleen in the two diseases. In the spleen 
of splenic anaemia there is extensive fibrosis of the splenic pulp and 
Malpighian corpuscles; while in the enlarged spleen of rickets, as 
far as I have had the opportunity of seeing, the fibrous increase is 
chiefly in the trabeculae, very little in the splenic pulp, and the 
Malpighian corpuscles remain unaltered, or are even hypertrophied. 

Again, it has been considered that congenital syphilis plays a 
very prominent part in the production of these cases of infantile 
ansemia with enlarged spleen. Not only was there no trace of 
syphilis in these two childi*en, but the other children of the same 
pregnancy remained quite healthy, the first case being one of twins 
and the second one of triplets. 

The disease to which these cases of splenic anaemia seem most 
closely allied is anaemia infantum, pseudo-leuchaemia, and doubtless 
some of them have been described under this name ; but in this 
condition, as described by von Jaksch, there is enormous increase 
of nucleated red corpuscles and marked excess of leucocytep, 
neither of which changes was found here. 

In cases of splenic anaemia haemorrhages are common. Epistaxis 
is the most frequent. West describes retinal haemorrhage and fatal 
bleeding from a tracheotomy wound; haematemesis and spongy 

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gums are mentioned by Bruhl. Williamson aud Miiller both 
describe a single deep ulcer of the intestine which was probably 
due to a primary hfiemorrhage into the mucous membrane, such as 
was evidently the cause of the multiple ulcers in my first case. 
These cases of hsemorrbages due to splenic aneemia all occurred in 
adults, and I can find no other recorded case of hsemorrhage of 
the dura mater due to this disease. April ISth, 1899. 

3. Cystic disease of the supra-renal gland. 
By Baymond Crawfued, M.D. 

THIS specimen, the left supra^reual, was removed from a patient 
under my own care, who died in the Royal Free Hospital. 
She was an elderly woman with chronic valvular disease, general 
arterial degeneration, and renal cirrhosis — the combined producta 
of rheumatic fever in adolescence and drink in the later years of 
her life. There were no symptoms in life to indicate any lesion of 
the supra-renal capsules. Post mortem, over and above the condi- 
tions already mentioned, there were several cysts of varying sizea 
on the surface of each kidney ; these cysts were those commonly 
seen in renal cirrhosis. The right supra-renal appeared quite 
normal. In the upper end of the left supra-renal was a two-lobed 
tumour, almost completely replacing that portion of the gland. 
The lower lobe of this tumour was about the size of a small walnut^ 
quite spherical, and also cystic; the cyst wall was tense, elastic, and 
for the most part translucent, but here and there on its inner 
surface could be seen patches of solid residue, some of which were 
more or less cretaceous. The cyst was full of a turbid, colourless 
fluid, which under the microscope showed some amorphous dihris^ 
but no booklets and no other foreign elements. The cyst was 
marked off by a clear capsule both from the healthy supra-renal 
tissue and from the contiguous solid tumour. This solid tumour, 
which was about the size of a hazel-nut, showed to the naked eye the 
ordinary appearance of supra-renal cortical tissue at its periphery^ 
but in its centre was soft and looked very fatty. 

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Under the microscope the cjst is seen to have a definite wall of 
fibrous tissue ; this wall separates the cyst also from the solid 
tumour. On the inner surface of the cjst wall are thin patches of 
solid tissue ; these patches show from without inwards every grada- 
tion from the normal tissue of the supra-renal cortex to simple fat, 
in which no trace of specialised cells is to be seen. The solid tumour 
shows just the same replacement of normal supra-renal tissue by 
fat, and only at the extreme verge of the tumour can one make out 
a few polyhedral cells in groups and columns. These appearances 
make it pretty obvious that the cyst was originally a solid tumour 
that has undergone fatty degeneration with liquefaction and forma- 
tion of a cyst. This confirms Virchow's suggestion that cysts of 
the supra-renal may be derived from degeneration of adenomata. 
The existing solid tumour is presumably an adenoma, if that term 
may be expanded to cover a localised hyperplasia of gland tissue. 
The presence of so well-marked a fibrous envelope around both 
cyst and solid tumour seems to me to present a difficulty that re- 
quires explanation. At the outer surface of each tumour this 
envelope is clearly the fibrous investment of the supra- renal capsule; 
perhaps the tumours have grown in accessory supra-renal bodies, 
which lay in tbe fibrous capsule of the supra-renal gland. As these 
accessory bodies have enlarged they will have expanded the fibrous 
capsule around them. The examination of a few normal supra- 
renal glands will show that this is a very common site of accessory 
gland tissue, and adenomata are well known to originate frequently 
in these accessory bodies. 

Cysts of any kind in the supra- renal capsules are very rare, 
Hydatids and blood-cysts have both occasionally been noted. I 
can, however, only find a single record in the literature of morbid 
anatomy of a cyst of the kind I have described. That was ex- 
hibited by Dr. John Ogle at the Pathological Society of London ; 
and in the volume of 'Transactions ' for 1865 is recorded "A Cyst 
in the Left Supra-renal Capsule, about the Size of a Boy's Marble, 
having almost Transparent Parietes, and containing Turbid Serum." 
Dr. BoUeston, in * AUbutt's System of Medicine,' alludes to ** a cyst, 
the size of a cherry, containing tenacious fluid." 

This specimen is now in the museum of the Boyal Free Hospital. 

Jcmuary 17 th, 1899. 

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4. Cyst of the supra-renal body. 

INHERE was a cjst in the right supra-renal body as large as a 
cherry, the contents of which were somewhat gelatinous, and 
free from any sign of past extravasation of blood. 

Microscopically the cyst wall is composed of firm fibrous tissue, 
with a few epithelial cells on its inner surface ; the substance of the 
supra-renal body appeared healthy. 

As to the origin of the cyst, it is probable that it was due to 
softening down of an adenoma. Adenomata composed of supra- 
renal ceils in a state of marked fatty change are by no means rare, 
and are sometimes found in a somewhat softened state. They are 
surrounded by a fibrous capsule, and the few cells attached to its 
inner surface in this specimen may be regarded as the remains of 
the diffluent adenoma. 

It was found on the post-mortem examination of a man aged 66 
years, who died with pneumonia and hemiplegia supervening after 
colotomy for a carcinomatous stricture of the upper part of the 
rectum. There were no secondary growths ; there was no evidence 
of the cyst in the supra-renal body being a softened second growth. 

January 17 th, 1899. 

5. Some lesions of the supra-renal in the insane. 
By Cecil F. Beadles. 

IIhib, the right supra-renal body, is the seat of extensive haemor- 
rhage, which infiltrates the whole organ, and in parts forms 
clots of some size. The adrenal is thus increased in weight to 
22*4 grammes, and its thickness is mostly affected. It is from a 
female lunatic, 13,421, who died February, 1899, aged 47, after acute 
melancholia of two and a half years. She had no symptoms 

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suggesting a lesion of this body. Having become greatly impaired 
in health, a few days before death she^passed into a collapsed state, 
weak and slow pulse, shallow breathing, cold extremities, and ex- 
pression of great illness, and she gradually sank. There were no 
other morbid chnnges iu the body ; blood-vessels were healthy. The 
left adrenal was normal. 

The supra-renal bodies have not been examined in the asylum 
with any regularity, but I have several times seen slight heemor* 
rhage in the organ, though nothing like so extensive as in the 
present instance. There are several other cases recorded in the 
autopsy books, of which the following may be mentioned. 

Female, 9497, died in 1886, aged 25. The subject of acute 
melancholia of three months' duration, wishing to die, constantly 
crying, and had to be forcibly fed. There was emaciation, which 
rapidly increased with great prostmtion, seized with faintness, and 
died soon alter. The right capsule was much enlarged with blood 
extravasation, the left to a less extent. All organs much congested* 
pneumonic consolidation of lower lobe of right lung, with recent 
lymph on pleura. 

Male, 10,411, died in 1888, aged 23, having mania of six weeks' 
duration, confused, rambling, hallucinations of sight and hearing, 
destructive to clothing. He was pale, thin, and admitted in a 
collapsed state, and died within two hours. Breathing slow, 
heart's action feeble, and extremities cold. Face of a pale yellow 
tint. Eyes directed towards the left, limbs helpless, temperature 
subnormal; Cheyne-Stokes respiration lasted for two minutes. 
Both supra- renals enlarged with blood extravasation. Decolourised 
blood clot almost filling right ventricle of heart, similar small clot 
in left; granulations on ventricular surface of aortic cusps. 

Male, 11,026, died in 1890, aged 63. The subject of acute mania 
of three months' duration, having wandering, extravagant delusions, 
noisy and restless. He had a dissipated appearance, and was fairly 
nourished. Died from exhaustion. Both sup ra-renals enlarged with 

Male, 11,106, died in 1890, aged 44. The subject of mania of ten 
months' duration, the cause of which was assigned to drink and 
overwork. Expression vacant, noisy, singing incoherently, making 
grimaces and gesticulations, faulty habits, knee-jerks exaggerated. 
He was thought to be a oise of general paralysis, and had had a 
fit «ome months before, followed by numbness on the right side, 

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aod great pain in the top of bis bead. Fairly nourished, eyes 
prominent, but pupils equal. A fading papular eruption on trunk. 
-Died from ezbaustive diarrhoea. Haemorrhage into one supra-renal 
capsule was found. 

Neither of the preceding cases had any signs of Addison's disease, 
but there were some symptoms which might suggest internal 
haemorrhage in an ordinary individual^ though in the insane little 
importance can be attached to those, ibr almost identical sym- 
ptoms may be present without any bsemorrhage being found after 

It has often appeared to me that the supra-renal body is par- 
ticularly liable to undergo atrophy, with, it may be, inflammatory 
changes in the insane, but my observations have been few. I 
regret to acknowledge that the condition of these glands has 
received but scant attention on my part. Now and again, however, 
I have found them markedly atrophied. They are then usually 
small and unnaturally soft, and it seems as though slight blood 
extravasation has taken place. Sometimes there is an early 
inflammatory condition present. In a few of these organs that I 
have submitted to microscopical examination small collections of 
round inflammatory cells were present amongst the epithelial cells. 
There has been nothing to pomt to such a lesion duiing life. Tbe 
specimen of which a section is shown under the microscope is such 
an instance. 

Male, 11,710, died with general paraly,8is of two and a half years' 
duration in 1894, aged 48. He had delusions of. wealth and 
position, speech blurred, tongue tremulous, gait ataxic, knee-jerks 
exaggerated; After a severe seizure became feeble and paralysed. 
To the naked eye the gland had a soft, dark, atrophied appearance. 
In microscopical sections there are seen small collections of round 
inflammatory cells between the columns of epithelial cells of the 
cortex, and also around vascular spaces in tbe medullary portion. 
In places are extravasated red blood-discs. 

One case of cyst of tbe supra-renal is recorded, but no details 
are given of the lesion. Male, 9228, who died in 1885, aged 38, 
from general paralysis of three and a half years' duration. Of 
vacant expression and eccentric behaviour, delusions that his flesh 
was dropping off, his heart had ceased to beat, and his bowels 
occluded. Hesitating speech, ataxic gait, exaggerated knee-jerks. 
Died demented. Of unhealthy complexion, and looked more than 

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his years ; had sore on his foot for five years, developed necrosis of 
several toes, and passed into a very feeble state. 

The number of instances of Addison's disease in Colney Hatch 
Asylum have been few. I have only found four instances in the 
autopsy books, though possibly others occurred. The majority lof 
the symptoms as a rule are more or less masked in the insane, but 
the chaiucteristic change of colour in the skin is usually weU 

Male, 6167, who died in 1875, aged 58, with mental symptoms 
of dementia of three and a half months' duration, brought on, it was 
supposed, by alcoholic indulgence. Complete loss of memory, in- 
capable of giving an intelligent answer, died after epileptiform 
convulsions. Haggard and looking prematurely old ; surface of 
body bronzed, more especially the chest. Supra- i-enals found 
fibrotic and partly calcified. Lungs healthy. 

Female, 7365, died in 1879, aged 22, after puerperal mania 
of two and a half months' duration following confinement four 
months previously. At first noisy and restless, then vacant 
and refusing to speak ; became listless and sat in a sleepy con- 
dition, incapable of attending to pei-sonal wants or cleanliness. 
Died after an epileptifoim attack. Though on admission she was 
well nourished, she rapidly emaciated and became pale and feeble. 
Skin assumed a dark and bronzed colour. Both supra-renals of 
large size and tough, but otherwise of "noimal appearance." 
Lungs riddled with tubercular abscesses from a nut to a walnut 
in size, and much pigmented fibrous tissue. 

Female, 9412, died in 1887, aged 35. A Jewess, with recurrent 
melancholia of three years' total duration, depressed and despond- 
ing, talked to herself and to imaginary persons, and wished to die. 
It was difficult to get her to eat anything but dry bread. At first 
in fair health, but pui-puric patches appeared on the legs. Had 
attacks of melana, began to lose weight and become feeble. 
Died from phthisis, the lungs being filled with abscesses and dis- 
seminated yellow tubercles. Left iliac vein thrombosed. Supra- 
renals large and gritty on section. 

Female, 12,147, died 1894, aged 57. Acute melancholia of three 
months' duration. In great terror with optical delusions and aural 
hallucinations. In a feeble condition on admission, and rapidly 
emaciated ; pigmentation of skin, especially around eyes and 
nipples, and other symptoms of Addison's disease present. 

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Supra-renals enlarged and caseous. Lungs and other organs said 
to be normal. 

tWhetber in years gone by cases have passed unrecorded I 
cannot say, but this is doubtful^ seeing that the last-mentioned 
one is the only case of Addison's that has occurred amongst the 
patients during the eight years that have immediately passed. In 
1893, however, a nurse died in the asylum with all the typical 
symptoms of Addison's disease. Both supra-renals were affected. 
They were much enlarged, fibrous and caseous in places, and con- 
taining calcareous particles. A section under the microscope 
shows the usual condition of the gland in that disease. The 
normal cells are replaced by fibrous tissue in a state of hyaline 
degeneration, and patches of caseous matter seen as granular and 
structureless areas. In parts where the degeneration is less 
advanced there may be seen giant-cells having the character of 
those of tuberculosis embedded in a round-celled inflammatory 
tissue. The neighbouring fat is in the condition usual to chronic 
inflammation of adipose tissue. There was no tubercle elsewhere 
in the body. 

A small benign tumour of the adrenal was published in ' Path. 
Trans.,' vol. xlix. Few cases of malignant disease involving the 
organ, whether primary or secondary, are on record. None of 
these presented the pigmentation of tbe skin peculiar to Addison's 
disease. In addition to the case recorded on p. 239 of the present 
volume, in which the supra-renala are affected by round-celled 
sarcoma, there are the following : 

Female, 4971, died in 1885, aged 35, being of Jewish bii*th, and 
the subject of epileptic imbecility for over twenty-six years, 
during which time, however, she had been out of asylum for some 
twelve years earning her living as a charwoman. Hands small 
and undeveloped, of weak intelligence, violent at times and had 
occasional fits. She was well nourished and in good health until 
the last year of life, when she became thin and developed signs of 
phthisis, having cough and hectic temperature, but np expectora- 
tion, the latter symptom being frequently absent in the insane. 
Her complexion assumed a sallow tint, the face slightly brownish. 
The liver was full of round, globular swellings^, soft on' section, 
with depressed peritoneal surface. Abdominal glands large and 
hard. Eight supra-renal, the size of a small orange but preserving 
its original shape, wks full of the same masses as the liver. The 

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left luDg is said to have contained tubercle ; pleura thickened and 
covered by lymph. Bight lung congested, oedematous ; bronchi 

Male, 11,182, died in 1896,aged 67. Recurrent mania with attacks 
extending over forty-seven years, assigned to alcoholism. Final 
attack lasting five and three-quarter years, during which he was 
incoherent, despondent, fancied he was rotting and full of poison. 
A dissipated, broken-down looking man, became, very feeble, and 
suffered from chronic bronchitis and asthma. A few weeks before 
death indications of mediastinal malignant disease developed, with 
growth extending above the right clavicle, and enlarged glands 
above the left. Attached to the right kidney was a malignant 
growth as big as an orange, involving the supra-renal body, in parts 
very hard, in others soft and disintegrating. The whole of lower 
lobe of right lung was breaking down and purulent, pleural cavity 
tilled with fluid. Enlarged glands at root of lung pressing on 
right bronchus and superior vena cava. 

In neither of the above cases were the growths examined micro- 
scopically. They bear a great resemblance to the case I show 
to-day, and it is very i)0S8ible they are of the same nature. It seems 
more probable that the lung of the first case was infiltrated with 
malignant growth, and not affected by tubercle. 

AprU 4dh, 1899. 

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Epithelial tumours, probably of congenital origin. 

By H. Radclifpe Crockeb, M.D. 

(With Plate VII.) 

MI88 G- — , aged 10, was sent to me by Sir John Williams for 
some growths on the forehead, and I saw her for the first 
time on November 16th, 1897. The parents stated that there was 
nothing present at birth, nor up to the age of three or four years. 
She had had a fall on the forehead, but the parents could not 
remember when the growths began in relation to the fall, or 
whether there was any connection at all. The first lesion was a 
pin*s-head spot, which increased very slowly up to two years before 
she came, when it became more active, and again they cannot 
remember how large it was two years ago. Eighteen months ago 
she struck it with a pump handle, and it has been more active 
since. When I saw her there was a congeries of growths extending 
from a quarter of an inch above the middle of the right eyebrow 
up to and about an inch beyond the hair margin. The lowest, 
which was the oldest, was about an inch square, but with irregular 
outline and nodular surface, as it was evidently composed of an 
aggregation of tumours from a hemp-seed to a pea in size, project- 
ing as a whole from a quarter to a third of an inch above the 
surrounding skin. It was soft to the touch, pale red in colour, 
with a few vessels over it, not tender or painful, but there was 
slight itching sometimes. Above this main growth, smaller single 
tumours from a pin's head to a hemp-seed in size went in vertical 
lines up to the hair. Just within the hair border was a large tumour 
about the size of a large bean. This one the parents said was 
growing actively; there was a pea-sized one above that. The 
tumours as a whole formed a vertical band about an inch wide 
between the brow and the hair. There was nothing abnormal in 

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Illustrating Dr. Radcliffe Crocker's case of Epithelial Tumours, 
probably of Congenita,l Origin. (Page 220.) 

Fig. 1. — Showing tamour substance continnous with sweat duct. (Obj. 1 in., 
oc. 1.) 

Fio. 2. — Showing the hair-foIHcle merging into the tumour substance in the 
deep part of the coriuin. 

Fia. 3. — Section of blood-vessel in the midst of tumour substance. The 
section also shows tlie structure of a lobule of the tumour. 

Fid. 4. — Cavities in the tumour substance with fragments of hair in them. 

Fio. 5. — Rudimentary hair-follicle and ? sebaceous gland showing early change 
in the hair-follicle into tumour structure. 

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- A 









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the general health, nor noteworthj in the family history. I was 
unable to form any opinion as to the nature of the tumours, but 
as they were obvious neoplasms, and not likely to yield to external 
or internal medication, excision of the two largest was recom- 
mended and carried out on the 18th, and ou the 29th the wounds 
had healed by primary union with linear scars. The remaining 
small tumours had also flattened down considerably. 

I have to-day heard from the family doctor that there has been 
no recurrence at the site of the lower tumour, but that close to 
the hair there is a nodule the size of two split peas, which is 
increasing in size. 

Microscopical examination with a low power showed that the new 
growth was almost entirely situated in the deep portion of the 
conum, and that it consisted of a congeries of gland-like lobules 
more or less completely separated by fibro-nucleated septa. There 
were also solitary nodules, sometimes above, but more often below 
the main masses of neoplasm, but never below the level of the 
sweat coils (Plate VII), fig. 1. With a higher power the individual 
lobules were seen to be made up of small epithelial cells, an outer 
row of elongated cells, and within roundish or irregular smaller 
cells, not very densely crowded ; in short, just the type of structure 
one sees in a rodent ulcer (fig. 3). The epidermis was unaltered. 

In the papillary layer also the changes were insignificant, viz. 
slight mitotic infiltration rather more marked near the main 
growth, and round the vessels ; changes could also be sometimes 
seen in the portions of hair-follicles and sweat ducts which 
traversed this portion of the cutis, of the same character as those 
deeper down. 

The sweat coils were doubtfully involved. It was common to 
find the new growth going close up to the sweat coils, the latter 
appearing to be quite normal. At the same time there were 
isolated portions of the neoplasm of which the general conformation 
and position suggested their origin in a sweat coil, but intermediate 
conditions I was unable to discover. As regards the sweat ducts 
the matter was on a different footing. There a transition from 
the normal duct into the tumour transformation structure could 
be clearly traced, the duct widening out, its boundary cells forming 
those of the lobule boundary, and the interior being filled with the 
small epithelial cells already described (fig. 1). 

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The hair-follicles were largely involved, and different stages 
could be traced in different sections ; in fact, the largest masses 
of the growth were round the hair-follicles, and in manj 
places could be shown to be from the hair-foUicle itself (figs. 2 
and 5). There were also cjst-like cavities in the midst of the tumour 
substance, which cavities contained portions of hairs (fig. 4). The 
part played by the sebaceous glands I was unable to determine. 
There were only rudimentary sebaceous glands,, and those few and 
far between. What there were appeared healthy, except that there 
was no fatty degeneration. Their absence perhaps suggests that 
they may have metamorphosed into the neoplastic structure, but 
there was no anatomical proof of it as there was in the hair- 
follicles and sweat ducts. In one section I found a rudimentary 
hair-follicle undergoing the neoplastic change at the root end, and 
two processes in the position of sebaceous glands, but not exhibit- 
ing sebaceous structure (fig. 5) . 

Blood-vessels.— TrsjiBT erne sections of blood-vessels could be 
seen in many of the lobules, the new growth involving the outer 
coat, but not the muscular, which was only thickened, nor the 
intima. These vessels often formed the centre of a system of 
lobules (fig. 3). 

Looking at the malignant microscopical appearance and the 
clinically benign nature of the tumours, and the imperfect develop- 
ment of the hair-follicles and sebaceous glands, it seems most 
probable that the tumours owe their origin to some embryonic 
defect in the development of the appendages of the skin, and 
probably a slight injury detennined their growth in this unusual 

I am not aware of the record of tumours with these clinical and 
microscopical characters, but shall be very glad if any members of 
the Society can give me references to any such case. This one 
illustrates well the fact that while the microscope is often necessary 
to elucidate the clinical appearances, the interpretation of the 
minute anatomical features is very likely to be erroneous unless 
the clinical history is known. 

March 21st, 1899. 

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1. Fibroma (congenital) from the neck of a child aged one year 
and eight months. (Card specimen.) 

Bj H. A. Lediajld, M.D. 

I^HE mother stated that the tumour at birth was the size of a pea, 
and continued to grow slowlj until January or February of 
this year, when it began to increase rapidly in size, and caused 
cough, hoarseness, and difficulty in swallowing. 

In the course of removal the tumour was found to lie high up on 
the right side of the neck and somewhat beneath the right ear, and 
behind but superficial to the sterno- mastoid muscle. The portion 
of the stemo-mastoid muscle subjacent to the tumour was some- 
what wasted from pressure. 

The tumour is about the size of a Tangerine orange, and is five 
inches in circumference. In structure it presents the characters of 
a pure fibroma, that is dense, fully formed fibrous tissue. No in- 
dication was present of any relation to muscle or nerve, and the 
tumour probably originated in fascia. The child made an easy 
recovery. May 16th, 1899. 

2. Adenoma of breast associated vnth cyst and calcareous 
degeneratioiu (Card specimen.) 

By Cecil P. Beadles. 

LEFT breast removed from a woman aged 60, under the impression 
she was sulEering from malignant disease. 
Thirty years ago the patient had milk abscesses in both breasts 

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after her first child, followed by scarlet fever fourteen days after 
her confinement. Both breasts were lanced, the left one' both to 
the right and left of the nipple. She had a second child two years 
later. A lump was first observed six years ago, projecting above 
the level of the skin to the right of the left nipple ; this disap- 
peared three years later, and then seemed to come and go until 
twelve months ago, since which it has remained and gradually in- 
creased in size. There was occasional lancinating pain, but no 
further discomfort. She was of a gouty nature, and subject to 

The tumour while under observation varied in size and consis- 
tency, and when softer marked induration was felt around. It was 
diagnosed as a cyst, but was believed to be undergoing malignant 
development on account of the induration, attachment to the skin 
and tension on the nipple, and from the presence of a hard nodule 
to the inner side of the breast, which appeared during the last four 
months. No glands were felt in the axilla either before or during 
the operation. 

The presence of a cyst was confirmed on incision into tbe parts 
removed, and this is associated with a small solid growth having 
some unusual characters. The cyst has a thick wall, and contained 
clear watery fluid of a slightly brownish-yellow tint. It is situated 
in the lower part of the breast, resting on the pectoral muscle, and 
is the size of a small hen's egg. Situated immediately behind tbe 
nipple is a small, roundish, distinctly limited tumour, about three 
quarters of an inch in its longest diameter; it is solid, fairly firm, 
white on section, and is surrounded by a distinct capsule that has 
become separated in parts by a blood-clot. More than half of the 
growth protrudes into the upper part of the cyst cavity, where it 
forms a white nodulated mass. It has attachments to the nipple by 
fibrous bands, which have caused retraction of that structure. The 
naked-eye appearance is that of a soft adenoma in which glandular 
elements are mainly represented. 

The hard nodule to the inner side of the nipple, already referred 
to, is found to be an irregular calcareous mass the size of an 
almond, that lies embedded in the superficial part of atrophied 
breast tissue close beneath the skin. Very little mammary tissue 
exists ; it is atrophied and replaced by fat. 

Embedded amongst the fat in the outer region of the breast and 
that extending towards the axilla are several enlarged lymphatic 

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glands. Thej are soft, and section does not show cancerous infec- 
tion, but a condition of fatty degeneration. The fat immediately 
around these glands is fiinner than that elsewhere, and on one side 
protrudes into the gland ; one of these glands was found beneath 
the edge of the pectoral muscle midway between the nipple and 
axilla. Examined microscopically the glands are in a condition of 
chronic inflammation, with partial replacement of the lymphoid 
tissue by fat cells; the surrounding fat is indurated by fibrous 
tissue. No trace of malignant cells can be detected. This condi- 
tion of fatty degeneration of lymphatic glands is not uncommon in 
chronic inflammatory diseases and wasting of the breast. I have 
also found it in some cases of malignant disease, and have 
described it elsewhere. It has also been referred to by Mr. Stiles. 

The microscopical structure of the tumour projecting into the 
cyst is that of certain forms of adenoma of the mammary gland, 
viz. one of the rarer forms of true adenoma. There is a fine stroma 
of connective tissue forming roundish spaces and clefts, which are 
mostly lined by a single layer of cubical or columnar epithelial cells. 
A few have much elongated cells, and some are filled with epithelium. 
In parts the alveolar spaces are crammed with the remains of 
degenerated epithelium. A thick capsule of fibrous tissue sur- 
rounds the growth. 

I am indebted to Dr. Charles Heaton, of Westgate, for the 
specimen, which is placed in University College Museum. 

May 2nd, 1899. 

3. Cystic disease of the breast in a boy aged three years. 
By D'Arcy Powbr. 

I DO not know how rare cystic disease of the breast may be in 
children, but I have never seen one before, and I think there- 
fore it is worth while to exhibit this specimen this evening, and 
the more so as it is the breast of a boy. 

The breast with the surrounding tissue weighs just over an 
ounce after it has been hardened in formalin and alcohol, and it 


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measures two and a half inches in length and breadth. The 
skin and nipple are absolutely healthy, the bulk of the swelling 
lying just below the nipple in the lower half of the organ. The 
section of the breast shows that a thick layer of fat is interposed 
between the skin and the pectoral fascia. The superficial portion 
of the fat is natural and of the usual consistency; the deeper 
portion is more loose, and contains numerous thin-walled cysts. 
The lai^st cyst is multilocular and roughly oval in shape. It 
measures after hardening an inch and a half in its long diameter, 
and one inch in depth. It has a definite but thin wall, bounded 
superficially by the subcutaneous fat, which is dimpled in every 
direction in its neighbourhood ; the deep surface of the cyst lay 
upon the pectoi-al fascia. The inner side of the breast is free 
from cysts, but on the outer side there are many cysts, each with 
a thin but definite capsule. The smaller cysts are less loculated 
than the larger ones ; all are filled with a clear yellow fluid. 

The patient was a healthy-looking boy aged 3 years, who was 
brought to the Victoria Hospital for Children on December 22nd, 
1898. He had always enjoyed good health, but eighteen months 
ago his mother noticed that the left breast was fuller than the 
right, and it had since slowly increased in size. The swelling had 
not been painful, nor had there been any discharge from the 

On examination a soft rounded tumour could be felt in the left 
breast. It was about the size of half a Tangerine orange ; it was 
cystic and adherent to the skin. The nipple was normal ; there 
was no definite edge to the tumour, and it was not tender. The 
axillary glands were not enlarged. 

The breast was removed by an elliptical incision made so 
obliquely across the tumour as to include the nipple, and extend- 
ing to the anterior border of the axilla. The tissues were then 
dissected away down to and including the pectoral fascia. There 
was very little bleeding, but even when the incisions were carried 
widely upon each side of the tumour many small cysts were cut 
into as they lay in the surrounding connective tissue. The wound 
had healed by first intention upon the tenth day. 

I suppose that this tumour would be classified as a case of sero- 
cystic disease of the breast, though there can be but little doubt 
that it is not a cystic tumour in the sense in which the term is 
applied to tumours of the adult female breast. It must be looked 

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upon rather as a cystic lymphangioma occurring in the connective 
tissue lying between the breast and the pectoral fascia, and it is 
thus comparable with the congenital cystic tumours found in other 
parts of the body in children, especially in the neck, where they 
have long been kiiown as hygromata. Recognising this fact, I 
should have been content to leave the tumour alone if the patient 
had been a girl, trusting in the hope that the functional changes 
taking place in her life might lead to its disappearance. But in this 
boy I had no hesitation in removing the breast, because the gland is 
f unctionless throughout life, and because its spontaneous disappear- 
ance, if it occurred at all, would necessarily be slow, whilst the 
mutilation performed at so early an age would become almost im- 
perceptible as the patient grew older. 

The specimen is preserved in the museum of St. Bartholomew's 
Hospital, No. 3142. Aj>Hl 4ih, 1899. 

4. " Butter '' cyst of the breast. 
By H. Betham Eobinson, M.S. 

MABY P — , married, aged 25, came under my care in St. 
Thomas's Hospital in October, 1897, giving the following 

Fifteen months before, three weeks after her first confinement, 
she suffered from an abscess of the right breast in almost the 
same situation as the present swelling. The breast became large, 
painful, and tender, especially at the upper and outer part. The 
inflammatory mass was punctured twice, not incised, and a con- 
siderable quantity of pus (?) was drawn off. 

Soon after the abscess had apparently healed she began to notice 
a small lump about the centre of the right breast. This quickly 
reached its present size, about that of a Tangerine orange, and has 
remained so since, having shown no sign of enlargement. There 
has been very rarely any pain in connection with it, and no dis- 
charge from the nipple. 

On admission the lump, which was circular in outline and about 

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two inches in diameter, was situated above the nipple, and showed 
at its inner part the scars of the two punctures. It was very 
elastic, and moved with the breast over the subjacent pectoral. The 
skin was free over it without any puckering ; there was no retrac- 
tion of the nipple and no tenderness on pressure. One gland on 
the inner wall of the axilla was distinctly enlarged. 

The lump, with a margin of healthy gland structure round, was 
removed, as well as the enlarged gland. 

The swelling proved to be a cyst with smooth walls, filled with 
a yellowish-brown semi-solid substance of the consistence of butter. 
On histological examination of the cyst wall there were gland lobules 
to be seen embedded in some excess of fibrous tissue ; the lining 
membrane was epithelial, flattened, and chiefly in a single layer, 
and not granulation tissue. 

The cyst contents hardened on exposure to the air. With ether 
the main part, fatty, was soluble ; the undissolved part showed 
microscopically protoplasmic masses, fatty epithelial cells without 
leucocytes, and also sheaves of circular crystals, probably stearine. 

The cyst, which arose after acute inflammation of a physiologi- 
cally active gland, was evidently due to one of two causes, a 
chronic abscess or the retention of secretion. The microscopical 
appearance of the cvst wall and the analysis of the contained fluid 
quite dispose of the former view. The cyst was a galactocele, but 
modified to this extent, that the watery constituents had become 
absorbed, leaving only the more solid parts behind. 

Modifications of galactoceles, although rare, have been duly 
recorded. Velpeau ^ says their contents may be partially coagu- 
lated, the watery part being absorbed, giving rise to a cream-like 
fluid. Billroth speaks of changes in the contents like those shown 
under the name of oily, buttery, or cheesy cysts. Such retained 
products might become quite hard, dry, and friable, resembling 
old cheese. Such a specimen was shown by Mr. Watkins 
Pitchford at this Society.* In his case the milk had been retained 
in dilatations associated with fibroid changes in the breast, and 
had gradually lost all its watery elements. The " cheesy " material 
was proved to be almost entirely fatty. October 18thy 1898. 

1 'Diseases of Breast,' New Sydenham Society, p. 241. 
« Vol. xlvii, p. 250. 

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5. A peculiar lipoma of the groin, {Card specimen.) 
By Cecil F. Beadles. 

APHOTOGBAPH was shown of a lipoma of the right groin, peculiar 
both in form and situation. It hangs as a loose pendulous 
tumour, not quite as large as one's closed fist, at the upper and 
inner part of the tliigh, having a wide base extending from the 
femoral ring to the root of the penis. 

It bears a singular resemblance to the scrotum ; it is but little 
larger in size, the skin is of the same loose puckered form, of a 
similar tint, and pubic hairs are continued over the base of the 
tumour. The likeness is increased by the feeling through the 
skin of a hard cord-like body running through the centre, and 
ending below in a small mass rather firmer than the remaining 
contents of the tumour. There is no dimpling of the skin obtain- 
able, as is usual in lipomata. The scrotum is natural, and contains 
two testes. 

An incision made into the tumour reveals only loosely lobulated 
fat, of a paler tint than that on the parietes. The hard cord referred 
to above is found to be a band of connective tissue, and the 
swelling below evidently a lobule of fat. There is no cavity 
within, and no hernial protrusion into the tumour; dissection 
proves the connections of the lipoma to be superficial to and 
entirely unconnected with the inguinal canal. 

It occurred in a man aged 78, who lately died in Colney Hatch 
Asylum with senile dementia of a few years' duration. So far as 
could be found out, he had had the tumour all his life, and it had 
only enlarged with the gradual growth of the body. 

AprU 4AK 1899. 

6. Large myxoma from the thigh, {Card specimen,) 

THIS tumour was removed from a woman 60 years of age by Mr. 
Bennett in St. George's Hospital. It had been growing for 
about six years and burrowed between the muscles in the upper 

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part of the thigh, but did not infiltrate the surrounding tissues ; 
it came away in many pieces, which were all encapsuled. The 
deeper part appeared to be connected with the linea aspera of the 
femur. The tumour probably arose from the intermuscular 
fascia. When collected and weighed it was 10 lbs. 15 oz., but it 
was heavier than this, for a good deal of fluid had by this time 
escaped from it. On section the tumour was glistening, and con- 
tained a number of cystic spaces with fluid in them. 

Microscopically it was a myxoma ; no cartilage or sarcomatous 
tissue was found in sections taken from various parts of the 
tumour. In its size and diffuseness it resembled a large but 
innocent cartilaginous tumour arising from the pelvis removed by 
my colleague, Mr. G. E. Turner, six years ago in St. George's 
Hospital. March 7th, 1899. 

7. Cysts in relation with an inguinal hernial sac in a woman. 
By H. Betham Eobikson, M.S. 

ANNIE P — , aged 23, single, was operated on by me in St. 
Thomas's Hospital on June 16th, 1897. She had been 
admitted in May with a strangulated left inguinal hernia, which 
was operated on and radically treated with complete success ; it 
was tben noticed that she had also a rigbt inguinal hernia. This 
hernia was small and easily reducible, extending as far as the 
pubic spine, but after reduction there remained a fulness suggest- 
ing thickening of the sac wall. 

At the operation an incision was made from internal ring to 
pubic spine, and on opening the sac gut was present and reduced. 
The lower end of the inner wall of the sac bulged into the cavity, 
and a prominent cyst was opened containing a brownish fluid ; 
into tbe wall of this one other smaller cyst projected. The sac 
was dissected up to the internal ring with the round ligament and 
the cystic swelling, and the radical cure completed. 

The cystic swelling proved to be made up of a number of 
varying sized cysts containing a dirty brownish fluid ; these were 
entirely retro-peritoneal, surrounding the round ligament. 

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Now as to the nature of these cjsts, there is very little informa- 
tion to be gained from surgical or pathological writings. Erichsen 
speaks of •* cystic tumours not unfrequentlj met with in the labia 
resembling inguinal hernia, but incompressible and irreducible, 
without impulse or coughing, and containing a dark turbid 
sanguineous fluid." There is no mention, however, of any asso- 
ciated hernia. I would suspect that possibly these cysts, which 
rather resemble my case clinically, have the same pathological 

To explain the nature of these cysts I think we can give a 
doTelopmental reason, which is that we have here an homologous 
condition to what has been described by Lockwood in the male in 
vol. xlvii of the ' Transactions,' only in his case the cysts projecting 
into the sac were pedunculated. In his paper he suggests that 
the origin of the cysts was from remnants of the Wolffian body 
situated in the cord retro-peritoneally. It does not seem extra- 
Tagant to suppose that some of the cellular columns of the 
Wolffian body may in the female be displaced and be dragged 
down into the canal with the descent of the canal of Nuck, for the 
frequent presence of the ovary in the hernial sac shows that in the 
female these retro-peritoneal structures can without difficulty pass 
into the inguinal region. 

Other views as to its nature would be that it is analogous to 
certain cysts that may be met with in relation with hemise, 
especially femoral, and possibly due to pathological adhesion of 
the serous layers, but the numbers and variation in size of the 
cysts are against this view. Then, again, we might consider whether 
it bears any relationship to cystic hygromata, which, although not 
uncommon in the groin below Poupart's ligament, have never, as 
far as I know, been described in the inguinal canal ; but a weighty 
argument against this view is that the cystic swelling was a cord- 
structure pure and simple, and dissected away easily in its entirety 
with the round ligament and its peritoneal process. Lastly, there 
was no evidence and no history of any preceding nsevoid formation 
to give rise to this by cystic degenerative change. To conclude, 
then, I would urge that there is no explanation more feasible than 
the first one I propounded. January 17^, 1899. 

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8. Multiple abdominal dermoids. 
By A. C. Latham, M.B. 

Two speciiueMB of multiple abdominal dermoids are shown, one 
a dermoid of the right ovarj, the other a dermoid in connection 
with the stomach. Both these specimens were removed from the 
body of a woman who had died from acute general peritonitis, set 
up by suppuration and perforation of the ovarian dermoid. There 
were also numerous other small dermoids in connection with the 
stomach, the descending colon, and the supra-renals. Nothing 
abnormal was found in the structure of the walls of these cysts, 
and no nerve-cells were observed. This condition is very rare, and 
extremely few cases of multiple dermoids had been recorded. 
Kolaczek, Fraenkel, and Hulke have each described a somewhat 
similar case. 

In discussing the nature of the above case, and considering 
whether such a condition should be regarded as being of a malignant 
character, reference may appropriately be made to a case recorded 
by Montgomery of a teratoma in which the author considered that 
the recurrence of the growth showed a malignant nature. But in 
the case shown to-night the weight of evidence points to the 
generalisation of the abdominal dermoid cysts as being due to cell 
transplantation, and not to malignancy as generally understood. 

November 16th, 1898. 

9. Myeloid tumour of neck. 
By H. J. Waring, M.S. 

THIS tumour was removed from a man aged 60, one who came 
under observation on account of a swelling in the left side of 
the neck. For at least forty-five years previously he had had a 
small tumour over the anterior border of the left stemo-mastoid 
muscle, and about one inch above the sternal extremity of the 

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clavicle. This remained about the same size until about one 
month before admission to the hospital, when it became painful 
and commenced to grow rapidly. 

When first seen there was a swelling, the size of a large walnut, 
in the lower part of the left side of the neck and over the anterior 
border of the stemo-raastoid muscle. The tumour was quite 
superficial, and appeared to be situated in the superficial fascia- 
It could be moved freely over the underlying deep fascia and 
muscle. The skin over it was bluish in colour, somewhat pigmented, 
and contained a number of dilated veins. The swelling could be 
lifted up, and the fingers made to almost meet behind it. It appeared 
to be quite solid and of uniform consistence. The lymphatic glands 
in the neighbourhood were not enlarged. 

The tumour was removed, when it seemed to be closely connected 
with the platysraa. On section it proved to be of firm white con- 
sistence, and eucapsuled as regards the posterior portion. Anteriorly 
it was attached to the deep aspect of the skin. There was no attach- 
ment of the tumour to the underlying deep fascia or muscles. On 
microscopical examination, the main poition of the tumour is seen 
to consist of a basis of fibrous tissue which contains numerous very 
lai*g6 mveloid cells, each having in it« interior numerous nuclei, 
and also a number of oval-celled sarcomatous elements. In a few 
places islands of hyaline cartilage are visible. The tumour evi- 
dently is a fibro-sarcoma containing cartilage and myeloid cells. 

Myeloid sarcomata are very unusual in the superficial tissues ; 
they occur most commonly in connection with bones. 

As regards the origin of this tumour there appear to be three 
possible explanations : 

1. The small tumour which had preceded the larger one may 
have been the remains of a branchial cleft, and in this there may 
have been bone and cartilage from which the tumour took its origin. 
This is the most probable explanation of the myeloid character of 
the tumour. 

2. A small portion of the sternal extremity of the clavicle may 
have been separated from the rest and displaced upwards. It then 
remained quiescent until from some cause active growth commenced' 
and gave rise to the formation of the tumour which was removed. 
In favour of this explanation is the fact that the tumour was 
situated entirely in the superficial fascia, and that it had no con- 
nection with the deeper tissues. 

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3. The small tumour which had existed for so long in the neck 
might conceivably have been a small dermoid cyst, and in the walls 
of this the myeloid growth commenced. Against this, however, is 
the fact that the tumour is quite solid, shows no trace of a cavity 
in its interior, and it does not contain any traces of bone or hairs 
in any part of it. 

As regards the malignancy of the tumour, this appears to be 
more marked than is usually the case with myeloid tumours. The 
tumour was removed with the surrounding tissues four months ago 
by Mr. Willett in St. Bartholomew's Hospital. Last week the 
patient returned with a distinct local recurrence of the growth. 

May 2nd, 1899. 

10. A case of multiple fibro-sarcomata of the scalp of nineteen 
years* duration; removal of growths ; subsequent recur rende 
in lungs. 

By Philip E. W. de Santi, F.R.C.S.Eng. 

LYDiA L— , aged 20, single, was admitted under me at West- 
minster Hospital in August, 1897, with multiple tumours of 
the right scalp. 

History of case. — The patient stated she had had swellings on the 
right side of the head as long as she could remember. Her mother 
informed me she first noticed the tumours when the girl was one^ 
year old. They came gradually, caused occasional neuralgic pain, 
and some of them slowly increased in size whilst others remained 
stationary. At no time was any spontaneous disappearance 
(** withering sarcoma ") noticed. The mother of the patient was an 
out-patient of mine with a gumma of the upper eyelid and other 
tertiary manifestations, but the daughter presented no signs, past 
or present, of cobgenital syphilis. 

The girl had been an in-patient in 1891, when one of several 
tumours of the scalp was removed : microscopically it was a fibro- 
sarcoma. She was again admitted in 1896. The note made then 
was ** A large fluctuating swelling and several smaller ones on the 
right side of the head ; two of the growths were removed and said 

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to be fibrous Ijmphomata ; there was much heemorrhage, which was 
stopped with Paquelin's cautery. Microscopically the growth was 
a fibro*sarcoma. 

Just prior to her third admission under uie she had noticed an 
increase in the size and number of the tumours and more pain. 

Her state was as follows : — a very loose condition of all the skin 
of the scalp on the right side, extending from the occiput to the ex- 
ternal angle of the right eye, and from the sagittal suture to the 
lobule of the ear. Tinder this loose skin could be felt a very large 
number of hard nodular masses, some large, others quite small. 
They were freely moveable over the subjacent parts and under the 
skin. At places between the hard masses were soft, almost fluctu- 
ating areas. These areas were painful to the touch. There were 
no enlarged glands, and the patient's general health was good. 
There was nothing discoverable in the lungs, liver, or other 

She had had prolonged treatment at various times with arsenic, 
iodide of potassium, <&c., but with no benefit. 

I determined to make an attempt to remove all the tumours ; 
my one trouble was likely to be heemorrhage. 

On September 8th I made two incisions : one in front of the ear, 
extending vertically from close to the sagittal suture to about one 
inch below the zygoma ; another about the same length posterior 
to the ear, with a slight concavity forwards. The skin was then 
raised off the nodular masses, which were removed in all directions 
as far as they could be reached, the part below the zygoma espe- 
cially being cleared out. The greater part of the temporal muscle 
had to be removed to do this thoroughly. A third incision was 
then made, connected at either end with the second, so as to remove 
an oval piece of skin which was redundant (vide specimen). The 
wound was then closed with horsehair sutures. There was, 
during the operation, considerable hcemorrhage, and as the patient 
became very faint I had to leave three or four nodules at the upper 
and under part of the stemo-mastoid muscle. 

She made an uninterrupted recovery, and was sent to a conva- 
lescent home September 24th. 

In the specimen handed round can be seen a large number of the 
tumours removed. 

I subsequently heard from the medical superintendent of the 
Ctimberwell Infirmary that the girl was an in-patient there, with 

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obscure lung mischief suggestive of either phthisis or new growths 
in the lungs. 

She died about six months after the operation, and at the autopsy 
there was very extensive secondary infection of the lungs. The 
left lung weighed 8J lbs., was almost entirely solid, and had fun- 
gated through the diaphragm. 

The right lung was the seat of one large growth, and generally 
dotted with small growths. The pleurse were also affected, the 
right principally, the surfaces of the ribs and diaphragm being 
studded with growths. There were no growths in the other 
viscera or bones. 

I have to thank Miss Webb, the curator of the Royal Free Hos- 
pital Museum, for the loan of tho specimens of the lungs. 

I have here to-night, therefore, the following specimens : 

Macroscopic, — (a) A number of the tumours as they were re- 
moved at the time of operation ; these will be seen to be definite 
encapsuled growths of vaiying sizes and density. (6) A piece of 
scalp excised, showing some of the growths loosely attached, 
(c) The left lung, {d) The right lung. 

Microscopic, — (1) Section of a piece of the growth removed in 
1891 (Dr. Hebb). It shows masses of round-cells enclosed in 
dense fibrous-tissue bands. 

(2 and 3) Sections of tough and soft parts of one of the 
growths removed in 1897. In both these sections fibrous tissue 
predominates, and the general appearances are more those of fibroma 
than sarcoma. 

I think the case is interesting from many points of view : 

First, the rarity of the scalp as a primary seat of the growths. 
Primary sarcoma of the scalp is uncommon, and I have been unable 
to find records of quite a similar case to mine. The only one at 
all like it is recorded by Dr. Conner, of Cincinnati, in the • Annals 
of Surgery,' 1888. 

His patient was a woman of twenty-five, who, fifteen years before 
consulting him, discovered at the back of her head a small hard 
lump the size of a bean. It remained stationary for about thirteen 
years, then enlarged coincidontly with a pregnancy. After de- 
livery there was rapid enlargement, and when seen by Dr. Conner 
the tumour was the size of a second head. It was removed, and 
weighed almost 5 lbs., and microscopically was a spindle-celled 
sarcoma. There was eighteen months' immunity, then coincidently 

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with another pregnancy there was a local recurrence. After con- 
finement the growth was removed, and weighed 7 lbs., and proved 
to be a mixed spindle- and round-celled sarcoma. 

Secondly, the very definite history of the duration and gradual 
increase of the tumours, namely, nineteen years. 

At no time whilst under observation by the surgeons who saw 
her during six years was there any disappearance of the tumours, 
as in the " withering sarcoma " case of the late Mr. Morrant Baker 
and Dr. Morgan Dockrell. 

Thirdly, the death of the patient after extensive removal of the 
growth from secondary involvement of the lungs. 

Fourthly, the varying microscopic appearances of the growths. 

The deduction in my opinion to be drawn from such cases is that 
no hard indolent lump or lumps should be allowed to remain, 
though even for years in an unchanging and unchanged condition, 
but should be freely removed ; for though probably benign to start 
with, in the future they become malignant, and finally kill by 
secondary infection and exhaustion. October ISth, 1898. 

11. A case of melanotic sarcoma with secondary growths of 
unusual size in the small intestine. {Card specimen.) 

By H. Campbell Thomson, M.D. 

THE patient in this case was a man aged 49. He was a painter, 
had suffered from lead colic, and seventeen years ago he had 
a severe illness, which was said to have been called *' inflammation 
of the kidneys." 

Three years ago he noticed a sore forming under the big toe on 
the right side, which gradually got larger, and he went to the 
London Hospital, where he was told that he had a melanotic sar- 
coma. There the big toe was amputated, and at the same time some 
glands were removed from the groin. 

He remained free from symptoms for six months, and then began 
to mpidly lose flesh and complain of pains in the abdomen. He 
was admitted into the Middlesex Hospital early in 1899, under 

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the care of Sir Richard Douglas Powell. The chief symptoms were 
constant nausea, constipation, and ansBmia, with pain and tender- 
ness all over the abdomen ; there was no actual vomiting, and the 
constipation never amounted to complete obstruction. There was 
a large rounded mass to be felt in the left hypochondriac region, 
and an examination of the blood showed a considerable degree of 

The patient eventually died, and the result ottiie post-mortem exa- 
mination was as follows :— There was no local recurrence at the pri- 
mary seat of tbe growth. On opening the abdomen the left lobe of 
the liver, together with the intestines of that neighbourhood, were 
much bulged forward, but no definite grov^th was visible. I explored 
this region with my hand, and felt a huge tense swelling, which, 
however, immediately ruptured. This proved to be a cyst situated 
between the folds of the small omentum, with its walls closely ad- 
herent to the under surface of the left lobe of the liver, the under 
surface of the diaphragm, and the anterior wall of the stomach, the 
adhesions to the last named being very strong. This cyst con- 
tained about two pints of very dark brown fluid ; its walls were 
deeply pigmented, and in some parts were very thin and easily 

There were twenty large secondary growths in the small intestine ; 
the smallest was about the size of a marble, while the largest was 
about as big as a pigeon's egg. All these were growing into the 
lumen of the bowel, and only showed externally as small dark 
depressions which gave no idea whatever of their actual appear- 
ance or size. These were entirely confined to the small intestine ; 
the uppermost one was situated at the end of the duodenum, and 
the lowest one was at the ileo-caecal valve, while they were most 
numerous in the upper part of the jejunum. There was a varying 
amount of pigmentation present, and some hsemorrhage had 
occurred into tbe substance of some of them. 

There was a large deeply pigmented gland in the right groin, 
which on section showed cystic degeneration, and contained a dark, 
thick, semi-solid substance. 

Another similar gland was situated at the bifurcation of the 
tracbea, which also contained a similar substance to the last. 
There were no other secondary growths elsewhere. 

The chief interest in tbe case lies in the distribution of the 
growths, the tendency to formation of large cysts, and the great 

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size which the growths attained in the small intestine. The cyst, 
as the specimen shows, was of great size, and had the patient lived 
a little longer it would undoubtedly very soon have ruptured. 

With regard to the intestines, it is interesting to note, firstly, 
that all the nodules grew into the lumen ; and secondly that, con- 
sidering their number and size, they gave rise to very few sym- 

Lastly, the general distribution of the secondary growths in this 
case is somewhat peculiar, for, considering the advanced stages 
which they have attained in the small intestine, it might have 
been expected that there would also be some in the liver and 
other organs. This, however, was not the case, and with the 
exception of some slight enlargement and hardening of the glands 
in the lumbar region there were no other signs of growth besides 
those mentioned above. March 21«<, 1899. 

12. Round-celled sarcoma involving the region of the pancreas^ 
the supra-renals, liver, and left lung, {Card specimen.) 

By Cecil F. Beadles. 

MALE, 12954, aged 64, was admitted into Colney Hatch Asylum 
on October 2l8t, 1898, with melancholia of seven months' 
duration, tbe cause of which was unknown. He is described as a 
labourer, but had been an iumate of the workhouse for some 
months, and while there had accused other inmates of attempting 
to poison him. He was admitted in impaired health, with physical 
signs suggesting bronchitis and emphysema of both lungs. Being 
very deaf, and mental faculties much impaired, it was difficult to 
get anything from him beyond tbe above delusion. 

In tbe early part of December he went to bed with cough and 
general feebleness. Except for hsemorrhoids he was not known to 
be suffering from any disease beyond the condition of his chest. 
There was no rise of temperature, and he complained of no pain. 
There was nothing to suggest a thorough examination of the 
abdomen. He was fairly nourished and took food pretty well, but 

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he continued to get weaker, breathing more troublesome, and 
towards the latter part of January his feet began to swell. 
Urine was found to contain a trace of albumen. Mentally he grew 
more demented, and died January 25th. 

Autopsy. — Brain somewhat wasted, pia-arachnoid membrane 
slightly thickened over both cerebral hemispheres, and excess of 
fluid in tbe skull. Heart a little hyper trophied, but the valyes 
healthy ; a very slight degree of atheroma of the aorta; some fluid 
in the pericardial cavity. 

Both lungs firmly adhered to the chest wall. The right lung 
weighed 27 oz., and contained frothy fluid. The left lung was 
covered by thickened pleura; it weighed 33 oz., and was con- 
solidated throughout. It was pervaded by dense fibrous bands 
and infiltrated by new growth of a whitish colour, and in parts 
was much pigmented. The lung was seemingly invaded from the 
region of the root and base, and the bronchi and vessels as they 
emerged were embedded in growth. From this neighbourhood a 
deposit protruded into the upper part of the pericardial cavity, and 
there were deposits in the diaphragm beneath the lung. 

On opening tbe abdomen an entirely unsuspected condition met 
the eye. Tbe anterior part of the)cavity was occupied by the liver, 
enormously enlarged, the anterior edge reaching to the brim of the 
pelvis, and the organ completely covering the bowel. Its surface 
was a deep purple colour, scattered over with small round deposits 
of malignant growth, for the most part less than an inch in 
diameter, of pale yellowish-white tint, only slightly raised on the 
surface of the organ. On raising the liver there were no adhe- 
sions to the intestines, but it was firmly attached at the hinder part 
of the under surface of the right lobe to a mass of new growth 
which extended to the right kidney and over the front of the spine 
behind the duodenum, occupying the site of the pancreas. It was 
removed by cutting through the growth beneath, and was found to 
weigh just over 100 oz., measuring 12 inches across and a little 
over that length from posterior to anterior edge. The enlarge- 
ment was mostly of the right lobe ; posteriorly this was greatly 
thickened, and section revealed a malignant deposit having a 
diameter of over 6 inches, the central portion of which was soft 
and breaking down. The organ tapered away to a thin anterior 
margin and left edge. Throughout were various-sized deposits, 
both superficial and deep, varying in size from a pea to a large 

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liorse-cbestnut ; the centres of the larger deposits were softening, 
and in some there was a cavity with a ring of firm white growth 
around. The gall-bladder contained bile but no gall-stones. 

The kidneys, pancreas, stomach, and duodenum with the growth 
were removed entire, and afterwards more carefully dissected, and 
these are exhibited together with the left lung and portions of the 

The stomach is much contracted and its walls thickened, but 
free from growth. The duodenum, as was likewise the remainder 
of the intestine, is natural, and there were no deposits in the lower 
part of the peritoneal cavity. The spleen has been detached ; it is 
small, weighs 4 oz., and contains no new growth. Both kidneys 
are diseased; there are numerous superficial cysts beneath the 
capsules, filled with straw-coloured fluid, and there are a number of 
small round infarcts iu the cortical region, varying from a pin*s 
point to the size of a pea, probably of a malignant character. The 
left supra-renal body is of noimul size and shape, but section reveals 
a number of small, pale, wedge-shaped infarcts in the superficial 
portion. The right supra-renal body appears to be replaced by 
an enormous deposit of new growth partly embedded in the kidney ; 
it is of circular form, with a diameter of 2 inches, firm and white 
on section, and connected anteriorly with the growth beneath the 

Stretching across between the kidneys and occupying the site of 
the pancreas is an irregular mass of new growth. It is connected 
on the right side with that of the liver and adrenal, and has 
an outlying large mass of growth, which presumably originated in 
lymphatic glands around the pancreas and small curvature of the 
stomach. Everywhere it is white and somewhat soft on section. 
A small portion of growth protrudes into the inferior vena cava 
from the right renal branch. 

As for the pancreatic gland, at first it seemed probable that this 
was entirely replaced by new growth, and it was thought possible 
that the malignant disease had started in that organ. But this is 
evidently not the case. The pancreas has become displaced in a 
most remarkable manner, presumably by the growth pushing it 
over to the left ; it has there come to lie between the stomach and 
the left kidney, with its long axis from above downwards. The 
upper portion, which is compact and firm, is in contact with and 
reaches above the level of the left supra-renal ; the lower part is 


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tbianed aud spread out. There is no sigD of new growth in this 

Microscopically the growth is a round-celled sarcoma. Every- 
where the minute structure is the same with but slight modifica- 
tions, a mass of small round cells with a fine branching reticulum 
without any true alveolar arrangements. Blood-vessels are prac- 
tically absent. 

Sections from what was at first believed to be the head of the 
pancreas reveal no trace of that gland, there is nothing but 
deeply staining small round cells ; small blood extravasations occur 
in places. There are a few narrow connective-tissue bands, but 
the branching reticulum is very fine. Small growths in the liver 
are the same ; in the larger ones the cells are necrosed. A section 
of the large deposit in the right supra-renal shows a more necrosed 
growth. There is more fibrinous stroma, but the intervening cells 
are all spherical in outline. A few small thin-walled blood-vessels 
are seen amongst the cells. The small infarcts in the left supra- 
renal are composed of round cells. The lung is pervaded by 
bands of fibrous tissue in which is much pigmentary deposit. The 
walls of what few air-cells remain are greatly thickened, and the 
cavities are filled with a pneumonic deposit ; others are occupied by 
round cells similar to those of the new growth elsewhere in the 
body, and these cells infiltrate the fibrous tissue almost through- 

As to the site of origin of the growth, this would seem to have 
occurred either in the right supra- renal body or in the lymphatic 
glands, about the base of the liver and head of the pancreas. 

Apnl 4iK 1899. 

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13. A case of umbilical papilloma which showed some activity 
of growth in a patient fifty years of age, and which was 
due apparently to the inclusion of a portion of Meckel's 

Bv Charles D. G-been. 

THE specimen consists of the umbilicus from a woman aged 50 
years, whicli was removed by operation. Instead of the normal 
depressed cicatrix there is seen a solid slightly projecting growth 
with a warty-looking surface, and about the size of an ordinary 

The patient had complained of irritation about the umbilicus 
for about two years and a half before tbe operation, with ac 
occasional discharge of a brown colour. I first saw her on 
account of this about fourteen months before the growth was 
removed; there was then some eczematous irritation of the 
skin in the neighbourhood of the umbilicus, but no projecting 
growth was at that time observed; the bottom of the umbilical 
depression had an irregular warty appearance, which I thought 
was the result of irritation ; the surrounding eczema soon yielded 
to treatment, but there was from time to time an irritating 
discbarge from the umbilicus, which tbe patient declared was 
always worse during her menstrual periods. Having in mind the 
possibility of the development of an epithelioma I suggested 
removal of the umbilicus. Owing, however, to the illness and sub- 
sequent death of the patient's busband the matter was postponed. 
In August, 1898, 1 was again asked to see her on account of the 
umbilical condition, and there was then a projecting growth. No 
enlarged glands could be found. I asked Mr. Ballance to see her, 
and he agreed with me that the growth should be removed, not- 
withstanding the fact that there were some grounds for anxiety 
as to the administration of an anaesthetic. 

On September 2nd I removed the umbilicus with the growth and 
a portion of the surrounding skin ; the abdominal walls had about 
I^ inches of subcutaneous fat, the omentum was not adherent to 
the umbilicus, and no intestine was seen at the operation ; the peri- 
toneal surface of the abdominal wall presented nothing abnormal. 
The wound healed by first intention, and there has been no trouble 

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Examination of microscopical sections taken at right angles to 
the free surface showed that the skin surrounding the growth was 
normal ; the free surface of the growth presented a thick covering 
of stratified epithelium, the superficial layers of wbich had under- 
gone keratinisation ; this epithelium sent down-growing processes, 
and in places presented the appearance of flat-topped papilla for- 
mation. No cutaneous glands could be seen. 

The stroma of the growth was made up of fibrous tissue and 
un striped muscle, among which, without any definite aiTangement, 
were numerous glandular elements ; some of these were very near 
the free surface, others more deeply placed: they were for the 
most part tubular glands lined by long columnar epithelium with 
large deeply staining nuclei situated quite close to the basement 
membrane ; these glands were considered to be reproductions of 
Lieberkuhn's crypts, but differed from them in their exaggerated 
dimensions, some of them indeed being so large that they might 
almost have been described as cysts. Some of the glandular 
elements bore some resemblance to the mouths of pyloric glands. 
There were also found, but in much fewer numbers, glandular 
elements which were lined with a very short almost flattened epi- 
thelium, and which in a few instances contained colloid material, 
and looked not unlike the vesicles found in the thyroid body. 

I think there can be no doubt that the growth was developed 
from a remnant of the vitello-intestinal tract. 

Umbilical polypi of minor clinical importance, but which prevent 
the umbilicus from healing, are by no means uncommon in infants, 
and are familiar to all who have seen any considerable amount of 
midwifery practice. The application of a ligature or the section of 
the pedicle by the galvano-cautery in most instances readily effects 
a complete cure. A considerable number of them have been histo- 
logically examined and reported on, and they have been described 
under more than twelve different names ; they fall, however, into 
two divisions, those which are merely granulation tissue more 
or less developed into fibrous tissue, and those which show a 
mucous surface and the development of intestinal glands, and 
are derived from remnants of the vitello-intestinal tract. The 
literature of the subject shows that almost every degree of per- 
sistence of the vitello-intestinal tract has been known to occur 
from these small umbilical polypi causing no serious symptoms to 
the grave cases in which most of the intestinal contents are 

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discharged through an umbilical fistula due to a fully patent 
duct, or to the prolapse of tbe small intestine through a patent 

Specimens illustrating the histology of these minor intestinal 
polypi are described in the * Transactions * of this Society by Mr. 
Pearce Q-ould in vol. xxxii, and by W. S. Colman in vol. xxxix. 

In ' Pedriatics * for 1897 there is a paper by Dr. J. H. de Villiers 
on this subject, and in vol. ii of the same journal Mr. Charles 
Morton, of Bristol, describes the histology of two cases. In the 
same journal there is also a paper by Dr. Leonard Guthrie on a 
case of prolapse of intestine through a patent Meckel's diver- 

In the 'Illustrated Medical News* for 1889, Makins and 
Carpenter describe in considerable detail the histology of an 
umbilical polypus showing intestinal gland structure. 

Dr. Francis Villar, in a work entitled ' Tumeurs de rombilic,' 
published in Paris in 1886, gives a full account of all cases of these 
polypi published up to that date, but does not include as within 
the scope of his work intestinal prolapse and faecal fistula due to 
the persistence of Meckel's diverticulum. 

In * Archiv fiir Q-y nakologie,' Bd. lii, there is a description by 
Amdt of a most interesting case in which there was not only pro- 
lapse of iutestine through a patent duct, but also a separate 
pedunculated tumour which he describes as an entero-teratoma. 

In ' Langenbeck's Archiv* for 1895 Lowenstein gives an ac- 
count of a case on which he operated with a successful result, the 
tumour having been cut into under the idea that it was merely a 
granulation tumour; prolapse of intestine took place, and it was 
then referred to Lowenstein. Abstracts of several other cases are 
given in the paper. The most important of the other papers to 
which I have referred are by Kolaczeck in * Archiv fiir klinische 
Chirurgie,' 1875 (the first published paper on the subject) ; by 
Kiinster in ' Virchow's Archiv,' Bd. Ixix ; Siegfried van Heukelom 
in same periodical, Bd. cxi ; and by Tillmans in * Deutsche Zeit- 
schrift fiir Chirurgie,' 1883; by Lannelongue and Fremont in 
* Archiv g^nerales de medecine,' 1884; a paper by W. Ophiils 
entitled 'Beitrage zur Kenntniss der Divertikelbildungen am 
Darmkanal,' published in G-ottingen in 1895. 

My case differs from those, tbe accounts of which I have read, in 
that the free surface of the growth was covered with stratified 

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epitbelium, the superficial layers of which bad to some extent under- 
gone keratinisatioQ, and was not like the mucous surface of any 
portion of the abdominal intestinal tract, the glandular structures 
being chiefly in the deeper portions of the sections, and also in the 
history of the case and the age of the patient, all the other cases of 
umbilical papillomata having presented a history dating from in- 
fancy, and the patients being quite young, the oldest being thirteen 
years old (Tillmans' case), and the majority being only a few 
months old. 

I have not succeeded in finding a case quite like my own in which 
a growth of this nature first began to give trouble in late adult 
life, but Dr. Rufenacht Walters, in the * British Medical Journal ' 
for 1893, vol. i, gives an account of a case which, though probably 
of sebaceous origin, may possibly have been a case of this nature. 
He says, " A man aged thirty-four years consulted me on account of 
periodical attacks of slight stomach-ache followed by a little dis- 
charge from the navel; he had consulted another medical man, who 
had told him that he had a slight rupture at the navel. On 
examination I found a patent umbilicus leading to a skin pocket 
containing a yellow mass which the patient stated had been there 
for years; the mass was readily detached by a little careful 
probing, and proved to be composed of hairs and sebaceous material. 
The pocket was about 2 inches in diameter and i inch deep, 
with an opening of i inch. There was no hernia." It is expressly 
stated that the hairs were derived from a flannel belt he was wear- 
ing ; no further details are given, and it is not stated whether any 
re-accumulation took place. 

Villar, in the work to which I have already referred, gives 
details of eighty-eight cases of umbilical tumour of various kinds, 
but there is not among them one resembling my case in its histo- 
logical details occurring in a patient of advanced years; several 
cases of fibrous papillomata are mentioned in this series, one of 
which contained a small serous cyst, butin none of them are intes- 
tinal gland structure or muscular fibres described as having been 
found. The patients were from thirty to fifty years old. 

In the Clinical Society's 'Transactions' for 1898 there is an 
account by Mr. Battle of a case in which he removed an umbilical 
polypus which proved to have been an everted Meckel's diverticu- 
lum, and which was still connected with the intestine, from a child 
H years old ; the child died from scarlet fever shortly after the 

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operation, and the condition was verified by post-mortem examina- 

In the paper by W. Ophuls, previously referred to, references 
are given to most, if not all, of the cases bearing on the subject 
published up to 1895, among which are three cases of special 
interest, viz. that of Arudt, that of Lowenstein, and that of Tillmans, 
the references to all of which have been previously cited; in the 
case of Tillmans the secretion from the tumour was carefully 
examined, and was found to have an acid reaction and to have the 
power of digesting fibrin, and Tillmans considered that it was 
derived from a stomach diverticulum. Ophiils, however, in his 
interesting paper, which will well repay perusal, gives another 
explanation of the acid reaction of the secretion, attributing it to 
the influence of bacterial action on the exposed mucous mem- 
brane. February 7th, 1899. 

Beport of the Morbid Orotoths Committee upon Dr. Charles Oreen*s 
case oj^ umbilical papilloma in a patient aged fifty years. — We do not 
consider that this tumour is a papilloma. We agree in the main 
with the author's histological description, and we regard the growth 
as a columnar-celled carcinoma. Whether this is primary or secon- 
dary we are at present unable to decide. Should the absence of 
further symptoms show that the tumour was not secondary to an 
intra-abdominal carcinoma, we agree with the author's suggestion 
that it arose in Meckel's diverticulum. 

(Signed) D'Aect Power, 

March 2Srd, 1899. H. D. Eollbston. 

Some members of the Committee present who examined the 
specimen are not inclined to regard it as malignant. 

R. Q-. Hebb, Chairman, 

April 29tK 1899. 

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14.-4 case of substernal carcinoma. 
By W. S. Lazaeus-Bablow, M.D. 

rpnis specimen was removed from the body of a man aged 56 
JL years, who died in St. Q-eorge's Hospital under the care of 
Dr. Penrose. For three months previous to admission he had 
complained of "tightness in the chest," and on admission there 
were great dyspnoea and urgent cough. Examination of the heai-t 
showed some oedema of the cords and also of the tonsils and posterior 
pillars of the fauces, with some inflammation of the soft palate. 
The patient had occasional attacks of dyspnoea while in the hospital, 
one of which was so severe that tracheotomy was performed. The 
operation, however, did not greatly relieve the distress, and the 
patient died seventeen days after admission. 

The cause of the dyspnoea was not discovered until the sternum 
had been removed at the autopsy. It was then found that a growth 
about the size of a Tangerine orange lay obliquely in front of and 
pressed upon the trachea. The growth was not exactly placed in 
the mesial line, for though the upper portion lay on the right side 
of the middle line, the lower and more considerable portion lay on 
the left side. It occupied a space between the lower margin of 
the thyroid body and the upper margin of the fatty remains of the 
thymus, and was not connected anatomically with either of these 
structures. The growth had perforated into the trachea at a point 
in the middle line of the trachea one and a quarter inches above the 
bifurcation, and here a f ungating mass the size of a hazel-nut 
presented itself. This mass was situated one and a half inches helow 
the tracheotomy wound. There was enlargement of cervical lym- 
phatic glands, especially on the right side. Microscopically the 
growth was a squamous-celled carcinoma. 

BemarJcs. — The point of interest in this case has reference to the 
seat of origin of the growth. It is possible (1) that it arose in 
some embryonic remnant of epithelium included in the deeper 
structures during the closure of the branchial clefts ; (2) that there 
might have been a primary undiscovered mass of growth connected, 
for example, with the pharynx or other part of the upper alimentary 
tract ; (3) that it had arisen in an accessory thyroid body ; (4) that 

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it had arisen in connection with the thymus body ; (5) that it had 
arisen in connection with the trachea. Of these alternatiyes the 
first is regarded as the most reasonable, partly because it is probable 
that the main growth was here primary, and partly because of the 
difficulties in the way of the other explanations. Against the view 
that it was of thymic origin is that the remains of the thymus 
persist, and are in no way abnormal ; against the view that it 
originated in the trachea is the histological character of the growth, 
while there is really little beyond its situation in favour of its 
origin from an accessory tbyroid body. Nevertheless the possi- 
bility that a primary small growth may have been overlooked cannot 
be gainsaid, and it is of course quite impossible to prove definitely 
the view that has been adopted. It is interesting to note that on 
staining by Gram's method there is a complete absence of granules 
in the cells constituting the " cell-nests." Sbattock has shown that 
** dermoid " must be distinguished from " mucosal " cysts, and that 
the method of distinguishing between them is greatly aided by the 
fact that mucosal epithelium has no stratum granulosum, the eleidin 
granules in which are readily recognisable on staining by G-ram's 
method. The absence of eleidin granules in the cell-nests of the 
present specimen would argue that the embryonic remnant from 
which the carcinoma is supposed to have arisen was one derived 
from the pharyngeal mucous membrane during closure of the 
branchial clefts, and not one derived from the superficial skin. 

The specimen is preserved in the St. George's Hospital Museum, 
No. 7075. October ISth, 1898. 

15. Vacuolated carcinoma of the antrum. 
By H. D. RoLLBSTON, M.A., M.D. 

THE patient was a man aged 32 years, who first experienced pain 
on the right side of the face and lachry mat ions fifteen months 
ago. These symptoms were followed by swelling of the right cheek, 
which gradually increased. Ten months ago a tooth was extracted 
from the upper jaw on the right side and the antrum bored, with 
the result that half a teacupful of thick red fluid came away. 

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The tumour displaced the eye upwards, the palate downwards, 
encroached on the nose, and produced swelling of the face. Mr. 
Allingham, to whose kindness I am indebted for the specimen, re- 
moved the right superior maxilla. The antrum was filled by a 
soft white growth which has eaten its way through its bony 

Microscopically the growth is indistinctly divided up into 
lobules by delicate connective-tissue septa, which in places contain 
blood-vessels. In one or two places there are hssmorrhages. The 
general appearance of the gro^vth composing the lobules is that 
of an anastomosing network of delicate trabeculse enclosing round 
spaces. The trabeculse are composed of rather small round cells, 
arranged in two or more layers ; no fibrous tissue or vessels can be 
seen in these trabecule. The character of the cells is not, gene- 
rally speaking, definitely epithelial, though some of the cells lining 
the spaces appear cubical. Inside the spaces there is a homogeneous 
matiCrial which is presumably produced by the cells. In some of 
the spaces detached cells can be seen lying loose. 

The cells forming the trabeculse are in a good state of preserva- 
tion, and do not, except in a few sections, show vacuolation or 
manifest degeneration ; in some of the sections small spaces may 
be seen beginning to form inside large trabecules of cells. 

Towards the margin of the growth solid clumps and colimins of 
cells can be seen, and in some of these the gradual formation of a 
lumen can be traced. This part of the growth strongly suggests 

In some sections the epithelial-clad wall of the nasal cavity, with 
its ciliated cells in a good state of preservation, can be seen on the 
margin of the growth ; while sections through the outer wall of the 
antrum show the invasion and absorption of the bone. The ap- 
pearances are those of a small spheroidal-celled carcinoma of rapid 
growth, in which a peculiar change has taken place, leading to 
vacuolation of the epithelial columns and alveoli, A very similar 
appearance is sometimes presented in rather rapidly growing sphe- 
roidal-celled carcinoma of the breast, and may then imitate duct 

Tumours of this kind are described by Ziegler^ under the name 
of cylindroma carcinomatodes, who refers to a growth of this nature 

^ Ziegler, 'Text -book of Pathology,' translated by D. MacAlister, vol. i, 
p. 244. 

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in the lachrymal gland. Thoma ^ figures a growth exactly like this, 
and describes it as hyaline degeneration of a round-celled carci- 
noma of the mucous membrane of the antrum. This tumour, then, 
appears to be an atypical carcinoma in which a peculiar change of 
a presumably degenerative nature has taken place inside the alveoli. 
It probably arose from glands and not from the ciliated columnar 
epithelium lining the antrum, inasmuch as it is a spheroidal and 
not a columnar-celled growth. The degeneration might perhaps 
be more suitably regarded as allied to mucoid or colloid change 
than to hyaline, which is more associated with changes in connec- 
tive tissue. The term vacuolated carcinoma is suggested as being 
preferable to cylindroma carcinomatodes, inasmuch as it is not 
ambiguous, and describes the characteristic appearances. 

Apnl 4th, 1899. 

16. The final sequel to a case already reported of recurrent 
cystic disease of a supposed accessory thyroid. 

By Abthtjb E. Babkbb. 

IT appears to be highly desirable that cases presenting very 
unusual pathological features should be followed up to the end 
clinically ; and for this reason I desire to place on record a very 
short note of a case already reported to this Society in January, 
1896, and which has since terminated in death. With this final 
note we shall have a tolerably accurate record of the life history of 
a growth which appears to be comparatively rare, and which, though 
undoubtedly malignant, as the issue shows, had nevertheless 
existed for at least eighteen years. As to the rarity of the con- 
dition I may take a statement of Mr. Edmunds in the 1896 
volume of our ' Tiansactions,' p. 224. Bef erring to a case then 
reported by himself he says, **The only similar specimen to be 
found in the ' Transactions ' of the Society is one of * intra-cystic 
papilloma of an accessory thyroid gland,' described by Mr. Bilton 

' Thoma.,' Pathology,' translated by Bruce, vol. i, p. 607. 

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Pollard in vol. xxxvii (1886), p. 507." This happens also to have 
been a case of my own in which I operated at Universitj College 
Hospital, and upon which Mr. Pollard, our then surgical registrar, 
made the necessary microscopical examination, and reported it to 
this Society at my request. 

Besides these three cases I believe Mr. Bryant has somewhere 
put another on record, and the Morbid Q-rowths Committee, in 
considering my own case in 1896, refer to others alluded to by 
Woelfler in his treatise " Ueber die Entwickelung und den Bau des 
Kropes,*' Langenbeck's * Archiv f . klin Chirurgie/ Bd. xxxix, 1883. 

In reference to the malignancy of the case it is interesting to 
note that the structure and life history of this growtb lend sup- 
port to the axiom laid down many years ago by Virchow, i. e. that 
the more highly differentiated a neoplasm is, the less tendency has 
it to exhibit the characteristics of malignancy. Here we have a 
very complex structure of cysts and papillomata of the most bighly 
developed form, and with this very slow growth and very 
ra'oderate tendency to generalisation, and no cachexia. We know 
of its existence for at least eighteen years, and that at last it appears 
to have cut short the patient's life by what might be called an 
accidental extravasation of blood and pressure on the air-passages 
rather than by producing any particular dyscrasia. 

A very interesting report of the Morbid Q-rowths Committee, 
signed by Messrs. Berry, Bowlby, and Shattock, following my 
description of the tumour in 1896, leaves very little to be said as 
to its structure, but it is possible that the Society may think it 
desirable that this should now be supported by a further examina- 
tion of the recurrent masses since removed, and which I now present 
for supplemental research. 

The history of the case from the time of my report in 1896 is as 
follows : — The gentleman remained in good health from October, 
1895, to January, 1897. He then became uneasy about a recur- 
rence above the episternal notch, which more or less pressed upon 
the trachea and larynx. On January 27th, 1897, I set about re- 
moving this by excision, and found it as before, cystic. The cyst 
was about the size of a large walnut, and could not, unlike the 
previous recurrences, have been thoroughly excised unless I had 
with it removed part of the larynx with which it appeared to be 
incorporated, and this I decided not to do. I was obliged, there- 
fore, to plug the deep wound and allow it to close from the bottom. 

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This, to my surprise, it did readily though slowly and without 
much fungatioD, which I had expected from the part left behind. 
From this on until October, 1897, he was quite well. He then came 
to me for the removal of another nodule in the posterior triangle 
of the neck. This was easily excised, being freely moveable, and the 
wound healed per primam. Prom this time I have not seen him, 
but he has written more than once saying he was well. At the 
beginning of last August (1898) he appears to have suddenly 
developed a large hematoma in the left side of the neck, presuma- 
bly from rupture of some of the delicate vessels of the intra-cystic 
papillomata. A letter from his doctor (appended) is my only source 
of infoimation in regard to the extent of the swelling and cause of 
death, which appears to have been from apnoea. Dr. A. E. 
Norbum wrote, " The large tumour appeared suddenly on the left 
side of neck (extending to the shoulder) after a fit of sneezing. 
It was doubtless due to hemorrhage, subsided under treatment 
to a small mass the size of half a walnut, which was freely moveable, 
and was situated just above the subclavian artery. There were 
other small nodules in the neck, which, from their position, were of 
no immediate consequence. 

" There was nothing in the neck within our reach to account for 
his dyspnoea ; the larynx was depressed, and the trachea could not 
be certainly distinguished. On one occasion while examining him 
he gave two or three sharp coughs, and then, for an instant, the 
upper part of a mass which appeared to be enveloping the trachea, 
rose to the level of the epistemal notch. His health had been fail- 
ing for some time past.'' 

I believe no post-mortem examination was made. He had had a 
similar attack of breathlessness associated with the sudden appear- 
ance of a tumour over the larynx some years before, and was only 
sav«d from death by tracheotomy performed in the country. The 
swelling then noticed disappeared, and he seemed, when I next 
saw him, none the worse for it. It probably was due to a sudden 
effusion of blood, as in the last instance. 

I have no doubt that if we had all the published cases of this 
affection marked out carefully from beginning to end we should 
have important light thrown upon some of the questions of 
malignancy, not only of similar neoplasms, but perhaps of others as 

The clinical history of the earlier years of the growth until it 

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assumed the enormous proportions it presented when I first operated 
on it in October, 1889, together with an account of what was found 
at the opeiution, will be found in the 'British Medical Journal/ 
June 21st, 1890. January I7th, 1899. 

Eeport of the Morbid Orotaths Committee upon Mr. Arthur 
Barker* 8 specimen of cystic disease of a supposed accessory thyroid. — 
The tissue selected for examination was a circumscribed ovoidal 
tumour, which was removed on January 27th, 1897. In October, 
1897, a further series of tumours was removed, which have, on 
section, precisely the same macroscopic characters as the above. 

The growth is furnished with a fibrous capsule, in many places 
of considerable thickness, and consisting in such largely of fibri- 
fying spindle-celled tissue. The capsule is the seat of consider- 
able haemorrhage, both past and recent, and there is, moreover, 
wide-spread recent extravasation into the substance of the growth, 
possibly a result of the manipulation entailed by the operation. 
The tumour presents a complex system of narrow clefts holding a 
small amount of colloid and lined with exquisite columnar 
epithelium supported upon delicate septa of vascular connective 

That the growth (like those already described in the Committee's 
Report upon the previous specimens shown by Mr. Barker in 1896) 
is formed on the papillary type is evident from a study of its 
periphery. Here there occur considerable intervals where the 
substance of the tumour is altogether unattached to the capsule, 
which has all the characters of a cyst wall, being regular in con- 
tour and lined with a single layer of somewhat flattened epithe- 
lium, whilst the epithelium on the contiguous or the separated 
ingrowths is highly columnar. 

In certain situations the actual origin of the ingrowing system 
of processes is traceable from the wall of the cyst. The cells of 
the new growth retain their physiological property of producing 
colloid, a small amount of which occupies the narrow winding 
spaces between the complex system of papillary processes. In 
many spots the connective tissue forming the trabeculsB also con- 
tains colloid in which there occur the spherical vacuoles commonly 
seen in the normal secretion. 

Although the growth is bounded by a capsule, it is to be 
observed that in certain places the latter is in process of invasion. 

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and for this reason we class it as malignant, although, as the 
clinical history of the case proves, its malignancy is of an 
extremely low grade, as in the other recorded examples of this 
class of neoplasm. This invasion appears in the presence of 
minute epithelial extensions beyond the general contour of the 
tumour ; the youngest of these are yet solid, whilst others have 
acquired a lumen, precisely as described in the preceding Eeport,. 
already referred to. No lymphatic tissue was encountered in the 
sections, so that the origin of the growth in a lymphatic gland, 
though probable, is not demonstrated. In the case of the speci- 
mens examined on the previous occasion the lymphatic origin was 

(Signed) Jahbs Bbbby, 
a. a. bowlbt, 
Samxjbl G. Shattock. 

E. Q-. Hebb, Chairmcm. 
Apnl 2m, 1899. 

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1. The relations of chemical composition to germicidal action. 
By Jambs Ritchie, M.D. 

THE important relations which within recent years have been 
shown to exist between chemical composition and pharmaco- 
logical action suggested that similar relations might exist when 
the toxic action of chemical substances towards bacteria was 
concerned. The following paper gives the results of a few pre- 
liminary inquiries undertaken with the view of investigating this 
point. In these, only the power of substances actually to kill the 
organisms used was taken account of. 

The investigation involved the comparison of the members of 
groups of substances of allied chemical structure. In such a 
comparison it is necessary to ask how the action of a molecule of 
one body compares with the action of that of another, and the 
circumstances of the action of both must be as nearly as possible 
exactly similar. To meet the former condition solutions containing 
the substances in molecular proportions must be prepared. Such 
**noi*mar* solutions are of course constantly employed by the 
chemist, and were used all throughout this research. In the case 
of a salt they are obtained by dissolving an " equivalent " (i. e, the 
molecular weight in grammes if the metal be monovalent, half that 
amount if it be bivalent, and so on) in one litre of distilled water. 
In the case of organic bodies such as alcohols, aldehydes, phenols, 
&c., I have applied the term normal solution to one where the 
molecular weight in grammes has been dissolved in one litre 
of water. In fulfilling the second condition, namely, that the 
circumstances surrounding the actions of the bodies compared 
should be similar, many precautions had to be adopted. The first 

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requisite here is to have bacteria of nearly constant vitality. In 
the many investigations which have been made on various anti- 
septics the familiar anthrax-spore thread method introduced by 
Eoch has been much used. I adopted it in some of my experiments, 
but as many of the bodies investigated by me were very weak germi- 
cides, no results could be obtained with an organism in such a 
resistent form. In one or two cases, however, as will be seen, when 
this method was used the results were identical with those obtained 
when weaker organisms were employed. The typhoid bacillus is 
one of such weaker organisms, and has the advantage of not sporing. 
Old laboratory cultures grown at room temperature are of extremely 
constant vitality, and sub-cultures made from these and inoculated 
for twenty-four hours are similarly constant. Hence these were 
used for nearly all my experiments. The germicides must act on 
the bacilli in water, for if a substance such as bouillon, which 
contains organic matter, be used, a chemical union is apt to take 
place between the germicide and such organic matter, the result 
being that a certain amount of the former is as it were thrown out 
of court, and the amount of germicide available is diminished. 
This can easily be shown by making up solutions of the same body 
in bouillon and in water, and introducing bacteria. It will be found 
that it takes a much longer time for death to be effected in the 
case of the bacteria in the bouillon than with those in the water. 
Further, in comparing the action of such similar bodies as calcium 
and barium on bouillon, I found evidence that, per unit of time, 
combination with the organic bodies present did not occur in 
molecular proportions. This indicates how results may be vitiated 
if the precaution of using only such cultures of bacteria in water 
be not taken. Another point to be observed is that as nearly 
as possible the same number of bacteria be exposed to the same 
number of molecules of the body to be tested. In my experiments 
in any particular case the amount of germicide present was very 
great compared with the mass of bacteria to be dealt with, and 
though careful investigations were made no quantitative relations 
could be detected between the number of bacteria and the amount 
of germicide requisite to kill them ; but the vitality of individual 
bacteria in a culture varies between very wide limits, and it was 
found that if a very large number of bacteria were present, more 
time required to be allowed for all the very vital individuals to be 
killed. It is, therefore, expedient in all experiments to have as 


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nearly as possible equal numbers of bacteria subjected to given 
amounts of the substances to be tested. This was effected as 
follows : — An agar plate was infected with typhoid bacilli by 
smearing with a platinum loop, and was incubated for twenty-four 
hours at 37° C. The resulting growth was scraped off with the loop 
and shaken up in sterile distilled water. As numerous flocculi 
exist in such an emulsion, these were removed by filtering through 
a plug of sterile glass-wool held in a sterile glass tube. Equal 
moieties of the filtrate contained approximately equal numbers of 
typhoid bacilli. The general technique of the experiments was 
this: — ^A series of graduated dilutions of normal solutions or of 
fractions of normal solutions of each agent to be compared was 
made up, and about 1 c.c. of every solution placed in a test-tube. 
A minute drop (each drop being of the same size) of the typhoid 
emulsion described was placed in each tube ; at the end of the 
period of observation an eyelet from each tube was placed in 10 c.c. 
of melted agar, and the latter plated and incubated for twenty- 
four hours. The dilution in the case of each agent with which no 
growth took place was noted. Seeing that only comparative obser- 
vations were aimed at, in the results which follow no account is 
taken of the slight additional dilution effected by the water of the 
minute drop of typhoid emulsion added. The error thus introduced 
would evidently be the same for the same dilutions of the different 
agents, and therefore may be neglected. 

In some cases the technique was varied, in that instead of the 
dilutions of different agents requisite to kill a given number of 
bacteria being observed, the times needed for one given dilution to 
kill the bacteria were compared. In cases where both methods 
were tried with the same agents the results corresponded. The 
reason of this correspondence requires, however, further investiga- 
tion. It may be said that, while the experiment was in progress, 
in nearly ev^ry case the tubes were kept at the room temperature. 
In only a few cases was the action of the germicides aided by 

The general results of the experiments may now be indicated. 

1. The metals as germicides. — The only basis on which these can 
be really compared is by taking advantage of the groups which are 
formed under the periodic law of Mendeleeff, and even here we are 
somewhat hampered by the insolubility of many metallic salts. 

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(a) Calcium, Strontium, Barium. — The chlorides of these were 
used. Example : 

Shonn. 8 Loan. 4 hours. Tlioart. 
1 c.c. 2N CaCIj + V^ c.c. typboid emulsion . + ... + ... + ... 
1 c.c. „ SrCls + V& c.c. typhoid emultion . + ... + ... ... 
1 c.c. „ BaClj + 1^ c.c. typhoid emalsion . + ... ... ... 
1 c.c. '75 % NaCl-f i^^cc. typhoid emul- 
sion (control) . . . , . + ... + ,.. + ... + 

(The sign + indicates that growth took place; that no growth occurred.) 

(h) Magnesium, Cadmium, Zine^ Mercury, 

(a) The chlorides of these metals were used. Example : 

MgClj ceased to be efficient to kill a given number of organisms 
at \%% normal strength, ZnClg at -}^, CdClg at ^, while HgCl^ 
I'etained its potency to -^ normal strength. 

O) Nitrates. Here Hg(N03)2 required to be excluded, as it 
cannot be got in neutral solution in water without decomposing. 
Example : 

^^(NOg)^ in normal strength equalled in action a -^ normal 
solution of Zn(N03)2, and a t^ normal solution of Cd(N03)2 

As far as the comparative action of the metals was concerned the 
chlorides and nitrates gave similar results. 

Thus both in the calcium group amd the magnesium group a rise in 
germicidal power takes place with rise in atomic weight, 

(c) Lithium, 8odium, Potassium. --The nitrates were here used. 
Example : 

LiNOg in normal solution equalled in action NaNOg in 1*2 normal 
solution, and KNO3 in -^ normal solution. 

This looks like an exception to the above statement regarding 
the relation of germicidal action to atomic weight. It is interesting, 
however, to note that there are several other characteristics, e. g. 
the insolubility of its carbonate, in which lithium differs from the 
other members of the group. 

2. The acids as germicides, — The action of an acid atom in a 
group qud acid is well known. To prove its activity one need only 
say that whereas an ^^ solution of Na2S04 has no gennicidal effect 
whatever, an ^ solution of H2SO4 is a potent germicide. 

Interesting light is thrown on the cause of this activity when 
the group of fatty acids is considered. It is best to omit formic 
acid, as its reducing action introduces a new factor. Example : 

The following solutions were found of equal potency : acetic acid 

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y^ normal, propionic acid ^hs* butyric acid y^, valeric acid ^hs* 
caproic acid -^^. Comparing hydrochloric acid and acetic acid we 
find a y^ normal solution of the former equal in action to ^ 
normal solution of the latter. 

It is to be noted that in all these acids there is one atom of 
hydrogen acting as an acid, and the irregularity of its action is 
thus somewhat puzzling. 

Now if we compare the neutral salts of these acids we find that 
there is a regular increase of germicidal action with increase of 
molecular weight, the acetates being the least active. Example : 

The following solutions were found equal in action : potassium 
propionate 2*7 normal, potassium butyrate 1*5 normal, potassium 
valerianate *3 normal. 

The key to the apparent want of order among the acids is 
found in the fact that the germicidal action of the a^ids varies with 
the avidity of the add. The results of physical chemistry show 
that the order of germicidal potency given above for the fatty 
acids is precisely the order of their chemical avidity. If we take 
the powerful mineral acids HCl, HNOg, H2SO4, we find that they 
are nearly equal in activity, and also very nearly equal in germi- 
cidal potency. 

3. The halogens and halogen compounds as germicides, 

(a) Chlorine, bromine, iodine. (The solutions of these were 
carefully standardised against sodium thiosulphate immediately 
before use.) Example : 

The following solutions were found to have equal potency : 
01 Tir^ normal, Br -^^ normal, I i^foW normal. (The 
potency of the last was probably increased by the KI added 
to cause solution.) 

O) Hydrochloric acid, hydrobromic acid, hydriodic acid. 

Example (1). — (Anthrax threads :) 

Normal folntiont. 1 hour. 3 hours. 3 hours. 7 hovrs. 

HCl . . . + ... + ... + ... 

HBr . . . + ... + ... ... 

HI ... + ... ... ... 

HjO (control) . + ... + ... + ... + 
Example (2).— (Typhoid emulsion:) 

Normal solution. 1 min. 5 min. 15 min. 30 min. 

HCl . . . + ... + ... + ... 

HBr . . . + ... + ... ... 

HI ... + ... ... ... 

HjO . . . + ... + ... + ... + 

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These two experiments are interesting as showing that two 
different organisms under different circumstances give the same 
comparative results with the same agents. 

The general result is that with the halogens and the halogen deri- 
vativea increase of germicidal action is associated with increase of 
atomic weight. 

In connection with the acids mentioned it maj be said that 
their avidity as acids rather decreases with the atomic weight of 
the associated halogen. 

4. Comparison of the germicidal actions of methyl, ethyl, propyl, 
and htUyl alcohols with each other, and with that of the corresponding 
aldehydes and fatty acids. 

The following examples may be given : 

(a) Alcohols, — (1) Methyl alcohol 10 normal = ethyl 4 normal; 
(2) ethyl alcohol 2 normal = propyl normal ; (3) propyl alcohol 
normal =: butyl \ normal. 

(h) Alcohol, aldehyde, acid, — (1) Ethyl alcohol 5 normal = ethyl 
aldehyde -^ normal = acetic acid ^ normal ; (2) propyl alcohol 
normal = propyl aldehyde yV normal = propionic acid^^ normal. 

Thus among the alcohols, as among the neutral salts of the fatty 
acids, there is an increase of germicidal action vrith increase in 
molecular weight, 

5. The germicidal action of the cresols and diatomic phenols, — Only 
a few points were investigated here. 

(a) The cresols — ortho-, meta-, para-. The solutions having 
equal potency here were orthocresol ^\^ normal, paracresol ^^^ 
normal, metacresol ^^^j normal. 

It is interesting to note that in other chemical properties, such 
as melting-point, specific gravity, heat of formation, Ac, the ortho- 
body resembles the para- body, both standing slightly apart from 
the meta-. 

(h) The diatomic phenols — pyrocatechin (ortho-), resorcin 
(meta-), hydroquinone (para-). Here also it was found that the 
ortho- and para- bodies are about equal in potency, and stand some- 
what apart from the meta- body. 

From these very scanty and elementary observations it will be 
seen that there is some ground for belief that an important rela- 
tionship exists between chemical composition and germicidal 
action. The latter is apparently very complex, sometimes one 
part of a molecule playing a part, sometimes another. 

May 16th, 1899. 

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2, .On infections by unsound meat, more especially with regard 
to the Bacillus etiteritidis {Gartner). 

By Hebbebt E. Dubham. 

THOUGH it is possible that cases of illness caused bj eating un- 
sound meat may sometimes be due simply to the sterile 
chemical products of bacterial activity in the absence of living 
germs, yet hitherto no bacteriological evidence is available in most 
of such cases as have occurred. A majority of tbe recorded out- 
breaks with bacteriological evidence have been shown to be due to 
the Bacillus enteritidis,^ 

Serum diagnosis (jGhruber's reaction) as applied to cases of *' meat 
infection" — The results of the examination of two outbreaks have 
already been recorded by the author (one occurred at Hatton,^ in 
which the B. enieritidis was isolated, the other at Chadderton, 
Oldham).' Two further outbreaks have been examined, one at 
Surbiton, thanks to the assistance of Dr. Cooper ; the other at 
Salford, for which the author's thanks aFO due to Dr. Tattersall. 

In the appended tables are shown the results obtained by test- 
ing the serum of the patients about eight weeks after their illness 
upon a variety of cultures of the B, enteritidis. It will be seen that 
many of these serums give positive reactions of diagnostic import- 
ance, in that they clump the bacillus in comparatively high dilu- 
tions. More than fifty control observations show that *' normal" 

^ Tho following short abstract of the outbreak investigated by Q&rtner may 
be added. An ox was killed on account of diarrhoea, &c. ; ninety-three persons 
ate of the meat; of these fifty-eight became ill in consequence, and one of them 
died. The person who died ate a considerable quantity of the meat in an 
uncooked condition, and not long afterwards was taken with vomiting, &c.; 
however, he did not die until thirty-six hours after the meal. Tbe incubation 
period in this case is masked by the effects of surfeit. In the other cases the 
incubation periods were from twenty-four to thirty hours; the illness lasted 
three to five days in mild, and about four weeks in severe cases. The symptoms 
were nausea, vomiting, diarrhoda, weakness and prostration, fever, pains in the 
joints. In several instances the illness was followed by desquamation on the 
iiands and feet. Microscopical examination showed that the capillary blood- 
vessels in the meat were crammed with bacilli. By means of cultivation these 
bacilli were isolated, and found to be identical with a kind of bacillus which was 
present in large numbers in the organs of the deceased man. This bacillus was 
named the BctcUlus enteritidi* by Gartner. 

» • Brit. Med. Joum.,' 1898, vol. ii, p. 600. 

» Ibid., p. 1797. 

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human serum does not clump these bacilli at dilutions of 1 in 
100. On the whole the strongest reactions are given by the 
tests upon the yarieties ** Hatton " and " Giinther ; " less strongly 
upon " Psittacosis " and " S. P. 2 " (kindly sent by Prof. Lorrain 
Smith, from Belfast) ; and not sufficiently strongly for diagnostic 
purposes with ** Gartner" and **Morbificaos Bovis (of Basenau)." 
It' is to be concluded that the fever from which the patients suffered 
was caused by a variety of the bacillus closely resembling 
" Hatton " and '* Guuther." It will be seen in the table that the 
reactions given with typhoid bacilli are negative ; it is to be noted, 
however, that when the test was performed in the slipshod manner 
of mixing one drop of serum with nine drops of typhoid culture, 

Surhiton outbreak, August l^th, 1898. 

Note. — t means strong reaction ; • = slight reaction; tr. and ? = doubtful ; 
— = no observation. 

Date of teram, 

B. 16/10/98. 
1:20 . 
1:50 . 
1 : 100 . 

M. B. 16/10/98. 

1 : 100 . 

1 : 200 . 

1 : 500 . 
L. 10/11/98. 

1:20 . 

1:60 . 


C. 16/10/98. 
1 : 100 . 
1 : 200 . 

W. 16/10/98. 

1 : 100 . 

1 : 200 . 
R. 27/10/98. 

1 : 100 . 

1 : 200 . 

D. 23/10/98. 
1 : 100 . 




Girt. Giinth. Morb. P«U. Sp.3. Typh.H.S. Typli.W. Qwyn. 










t , 
? . 

t . 
tr. , 

t . 
t . 




, .. 




tr. ... 
















t .. 
t .. 



tr. .. 

t .., 

t ... 



t . 


... — 

— ... 
... — 

Total— 10 cases. 2 deaths. All survivors but one examined. 

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H., set. 16 years. 


19 ,. 


12 „ 


50 „ 


Became ill 34 bo 


For the following clinical notes I am indebted to Dr. Cooper : 

M.B. Incubation period 12 hours ; duration 19 days ; slow convalescence. 
„ 16 ,, », 6 ,, mild attack. 

»> " »» »» 15 )» 

Incubation period 20 hours ; duration 12 days. 
>» »> *^ i» »» ^ »» 

>f ft 15-17 »( n 5 „ 

Became ill 34 hours after performing post-mortem on one of the fatal cases 
H. N., 8Bt. 67 years. Incubation period probably 44 hours ; severe attack ; died 

on 8th day. 
£. C. 67 „ Incubation period probably 8 „ „ „ died 

on 4th day. 

Unfortunately no bacteriological examination of the fatal cases was made. 
The incubation and duration of the illness both point to something more than a 
mere intoxication with formed products, especially when taken with the serum 
reactions of the survivors. 

and observing the effect after half an hour, considerable clumping 
occurred ; a lantern slide from a preparation of the serum of M. B. 
(Table I) in which the reaction is almost complete (dilution 1 : 
10 ; time, half an hour) is shown. If this had been the only test 
performed the case would in all probability have been returned as 
" enteric fever." The varieties Hatton and Giinther are not very 
susceptible mutually to typhoid when tested by experimental or 
** natural" sera. 

The tables also show how mucb less differentiation is to be seen 
in the seinims which were tested in low dilutions. A case may be 
quoted which clinically appeared to be a case of enteric fever 
acquired by the consumption of oysters. Gruber's reaction proved 
negative at each of the five times during the course of the fever 
and during convalescence that serum was taken. The first was 
taken towards the end of the first week ; my observations har- 
monise with the recently published results of Kasel and Mann,^ 
in that I have never yet seen a diagnostic positive reaction at so 
early a stage. 

One of the later samples when tested by the " slipshod method " 
gave very considerable amount of clumping with typhoid bacillus, 
but also with the variety Gunther ; since these bacilli do not react 
readily mutually the result was of no diagnostic importance, and, 

* 'Miinchener med. Wochenschrift/ 1899, p. 681. 

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Mary Street, Salford outbreak, July let, 1898. 
Blood collected September 26th« 1898. 


. Morb. P«tt. Sp.9. Typh.H.8. Typh.W. Gwyu. 
... ? ... — ... — ... — ... ... 

Mrs. B. 




1:100 . 

. t .. 

. ? .. 

. t 

1:200 . 

. .. 

. .. 


Henrj', set. 9. 

1:20 . 

. t .. 

. t .. 

. t 

1:60 . 

. .. 

. .. 

. tr. 

George, jet. 7. 

1:20 . 

. t .. 

. ... 

. t 

1:50 . 

. .. 

. .. 

. ? 

Gertie, set. 5. 

1:100 . 

. t .. 

. .. 

. t 

1:200 . 

. .. 

. .. 


... tr. 

— ... — ... — ... 

• ... __ ... _ ... — ... ... 
... ... 
Total — 5 cases. 1 deiitb. All snrvivors examined. 
Note. — Some beef was bought on June 25th ; it was hashed and enten without 
ill effect on the following day. The remains were eaten cold before 9 a.m. on 
the 28th by the mother and four children (the father and babe of three months 
did not have any and were not ill). The mother was taken with htccongh about 
2 p.m. on the same dny, and later diarrhcba and vomiting set in ; exact onset not 
known (incubation not less than about six hours). She was in bed four days. 
Albert, set. 3 years, began vomiting in the night of 28th (incubation about 
twelve hours or more). Next morning diarrhoea ; great collapse ; died about 
thirty -six hours after the meal. The other children were taken ill about the 
same time, but they all recovered, one being in danger for some time. The 
illness whs ascribed to the thundery hot weather having affected the meat. 

as would be expected, trials with these and several other cultures 
in higher dilutions all gave a negative result. 

An outbreak of illness through eating pickled tongues occurred 
last summer at Atherton. Dr. Neech very kindly succeeded in 
obtaining two blood samples for me ; both of these failed to give 
any reaction, though tested upon a large number of varieties. 
Another negative result was afforded by ** M," who had eaten veal 
pie with " X " at lunch on one day without ill effect, but when 
the pie was finished the next day by "M" and "Y." both had 
slight diarrhoea lasting only twenty-four hours. " M's " serum was 
tested on the second and ninth days : it was, perhaps, too soon after 
the onset of the illness for reaction to have developed if really the 
illness was due to B, enteritidis ; laboratory experience shows that 
the acquisition of reaction may be much delayed after very slight 
doses of bacilli. 

It may be noted that the researches of de Nobele ^ completely 
^ De Nobele, " Du f ^ro-diagnostic dans Ics affections gastro-intestinales d*ori- 
gine alimentaire," * Ann. Soc. de M6d. de Gand,' 1899, p. 6. 

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confirm my obser?ations upon tbe relative strength of reaction 
towards different varieties of B. enierUidis as well as tbe fact that 
in insufficient dilution an erroneous diagnosis of enterica may be 

BistribtUion of the B. enteritidis. — Tbe identificatixin of a given 
microbe as tbe cause of a disease is really only the beginning of 
tbe knowledge requisite for tbe proper control of tbe disease ; we 
must also know its economy in nature. This is extremely difficult 
to work out in tbe case of bacteria. 

Apart from disease in man or anim&ls we do not yet know very 
much about the ultimate or outside life of the B. enteritidis. In 
connection with illness in man we know from the researches of 
Gartner, van Ermengem, Gaffky, Gunther, Hoist, Basenau, and 
many others, that the animals from which tbe meat was obtained 
were suffering from infections with B. enteritidis at tbe time when 
they were slaughtered. In many of tbe cases there was either 
puerperal trouble of cows, or septicsemic diarrhoea of calves. 
Bacilli have been recorded under various names which agree in 
their morphology and their cultural characteristics (especially 
their powers of acid and alkali formation, fermentation and 
serum susceptibility), and these we must regard as members 
of a well-defined group ; this may be called the group of tbe B. 
enteritidis. The following examples may be named bog-cholera 
bacillus of Salmon and Smith, B, typhi murium of Loeffler, 
B, psittacosis of Nocard, and tbe so-called pseudo-tuberculosis 
bacillus of several authors. All of these cause spontaneous epi- 
zootics amongst tbe different animals. There is reason to think 
that the bog-cholera bacillus has been communicated to man (e. g. 
tbe Middlesbrough epidemic), as also the so-called psittacosis 
bacillus. Tbe B, typhi murium is of interest from tbe fact that 
cultures of it are sold to be scattered about for tbe purpose of 
killing mice (especially field mice) ; according to Schmidt (Baum- 
garten's * Jabresbericbt,* xii, p. 513) 3063 cultures were sent out 
from the Dresden laboratory between October, 1895, and April, 1896. 

It remains to be seen whether these doings will have disastrous 
results for man. The fact that the so-called mouse typhoid and 
pseudo-tubercle in guinea-pigs arise spontaneouslv in laboratories 
is suggestive that tbe bacilli may be conveyed to them from 
without by means of the food ; in so far as some form of corn may 
be the vehicle, it may be mentioned that Wolffin has described an 

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organism (B, levans) in fermenting dough which is somewhat 
similar in ite cultural reactions to the B, enteritidis, but the 
account is hardly complete enough for justifying any certain 
conclusion. For the present we must leave the question as to how 
the cows, calves, pigs, &c., obtain their infections unanswered, but 
we should keep the fact that they do become infected before us, 
because we may be secondarily infected through their means. 

We must not rest satisfied in the knowledge that these inf ed^ions 
occur amongst our sources of meat, but must go further and 
determine whence the infection arose. In the case of an outbreak 
of swine plague Voges was able to determine deaths previously 
amongst the poultry, and also to find the microbe of swine plague 
in the skimmed milk with which the young pigs were fed ; still 
the question how the bacilli got into the milk remained un- 

Lantern slides showing the morphology and agglutinating reac- 
tions of the B. erUeritidis were demonstrated. 


Characters of B, enteritidis. — 1. Young agar cultures ; polymor- 
phous ; threads, bacilli of various lengths, and round coccus-like 
bodies (similar to typhoid bacillus). 

2. Gelatine streak cultures a few days old may show the charac- 
teristic forms whose ends do not stain (this was noted by Gartner) ; 
in recently divided individuals the stained material is all at one end. 
This appearance is not always obtained unless the culture is of the 
right age. 

3. Flagella maximum ten or more (similar to typhoid bacillus). 

Cultural characterUticM, 

1. Agar, gelatine, coagulated serum, Eisner's gelatine, potato and 
milk show nothing of diagnostic importance except the non-lique- 
faction of gelatine, and the non-coagulation of milk. 

2. Broth soon becomes turbid, and a pellicle and considerable 
deposit form. 

3. Litmus- whey becomes slightly acid (2*5^4 per cent, one tenth 
N NaOH) in the first two days at 37° C. ; about fourth day alka- 
linity begins (distinguishes from typhoid and colon bacilli). 

4. Peptone 2 per cent, with glucose or mannite, 0*1 per cent*. 

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becomes alkaline after a passing slight acidity (distinguishes from 
typhoid bacilli). 

6. Fermentation tests with 1 per cent, peptone and 1 per cent, 
various sugars; dextrose, levulose, maltose, dextrine, and manuite 
lead to acid and gas formation; gas formation distinguishes from 
typhoid. Lactose, cane sugar, glycerine, starch, and inulin are 
not fermented. (All colon bacilli ferment lactose and glycerine, 
Lactis aerogenes, Friedlander, <fcc., also ferment starch or inulin.) 

6. Milk with dextrose (2 per cent.) becomes highly acid, but is not 

7. Indigo carmine and litmus are readily reduced (like typhoid 
bacillus) when added to suitable media. 

Colonies on gelatine in the neighbourhood of colonies of B. coli 
communis are much inhibited; they may appear like colonies of 

Growth on old agar upon which the bacillus or B, typhi ahd, or 
coli has been grown have not afforded me satisfactory results. 

The following cultures have been examined : " Gartner," " Giin- 
ther," " Hatton," Psittacosis (Nocard), JBovw morUficane (Basenau), 
S.P. .2 (LorrainSmitb), Morseele, Gand, Calmpthoult (van Ermen- 
gem), Sirault (Herman), Aerteycke (de Nobele), Vienna, Typhi 
murium (Loeffler), hog cholera. 

I must express my gratitude to Prof. Gruber, Prof, van Ermengem, 
Prof. Flexner, Dr. Nicolle, Dr. Basenau, Dr. Gunther, and Prof. 
Lorrain Smith for kindly sending me cultures. 

May imh, 1899. 

3. Congenital tuberculosis in calves. 
By J. M^Fadyean, M.B., B.Sc. 

UNTIL within the last few years the opinion that tuberculosis is 
frequently transmitted from the parent to the unborn foetus 
was almost universally held by breeders of cattle and by veterinary 
surgeons. Nevertheless this belief was never justified by the 
evidence bearing upon the question. Needless to say, the only 
evidence warranting a belief in the frequency of congenital tuber- 
culosis would be the common occurrence of demonstrable tuber- 

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culous lesions in the bodies of animals newly born or so young as 
to preclude the possibility of the lesions having been poet-partum 
in their origin. Search for such evidence has shown that with 
comparatively rare exceptions calves bom of a tuberculous parent 
are free from any sign of tuberculous disease. That this apparent 
freedom from the disease is real has within recent years been 
abundantly proved by the application of the tuberculin test to the 
young progeny of tuberculous cows. 

The proportion of calves bom tuberculous has been variously 
estimated at from 1 in 10,000 to 3 per 1000. The former estimate 
was based on the results of the slaughterhouse inspection of 
calves under one month old in the Munich slaughterhouse, where 
from 20 to 30 per cent, of the adult cattle are tuberculous in some 
degree. The estimate was probably too low, owing to a consider- 
able number of slight cases being overlooked. The higher esti- 
mate has been given by Bang for Denmark, where from 30 to 40 
per cent, of the cows are, or until recently were, tuberculous. So 
far as I am aware only one instance of indubitably congenital 
tuberculosis in the calf had been put on record in this country 
prior to 1897, and that case was described by myself in the 
* Journal of Comparative Pathology and Therapeutics ' in the vear 

In the latter part of 1896, in consequence of a discussion which 
was carried on in the columns of the 'Veterinary Record,* I 
offered to pay the sum of one guinea for each new-bom tuber- 
culous calf forwarded to the Eoyal Veterinary College. Up to the 
present time that offer has brought me three undoubted cases of 
congenital tuberculosis in the calf. One of these I received in 
1897, and it has already been referred to in the 'Journal of 
the Boyal Agi*icultural Society of England ' (vol. ix, p. 126). The 
remaining two cases were received during the last seven months. 
Before describing these it may be of interest to note regarding the 
case already recorded that the cow which gave birth to the calf 
was the subject of very extensive tuberculous disease, including 
tuberculous metritis. 

Case I. — In this case I had not an opportunity to make a complete 
post-mortem examination, as only portions of the diseased organs were 
sent to me. A piece of skin and umbilical cord was also sent to 

1 Vol. iv, p. 149. 

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show that the calf was only a day or two old. No historj of the 
mother was obtainable. The following were the lesions noted : 

Liver. — This organ contained numerous tubercles rather smaller 
than barley grains. The hepatic lymphatic glands were enlarged 
to the size of a horse-bean, and on section they showed some 
streaks of caseation. 

Spleen, — The tubercles here were larger than those in the liver, 
but only about half as numerous. 

Lunge, — Tubercles about the same size as those in the spleen, 
but scarcely so numerous. 

Heart. — A piece of this organ comprising 2 inches at the apex 
and a portion of the outer wall of the right ventricle was sent, and 
it contained one tubercle as large as a pea. 

Histology. — All the tubercles had yellow caseous and partially 
calcified centres, around which they were composed of epithelioid 
and giant cells. Tubercle bacilli were sparingly present. 

Case II. — This calf was exactly a week old when killed. The 
mother was killed about the same time. The lungs of the cow 
were tuberculous, but no other lesions were observed. The uterus 
was not examined. The post-mortem examination of the calf 
showed the following lesions : 

Liver. — This organ had scattered through its substance some 
hundreds of yellow tubercles, somewhat smaller than barley 

Hepatic lymphatic glands, — These were enlarged to form a mass 
about the size of a small hen's egg. Their substance was 
mottled with white caseo-necrotic streaks. 

Spleen. — Normal in size, but its pulp contained upwards of 
thirty yellow tubercles, mostly about the size of barley grains. 

Kidneys. — Each organ contained a few yellow tubercles, rather 
smaller than those in the liver and spleen. 

Lungs. — About ten yellow tubercles as large as barley grains 
were present in the two lungs. 

Bronchial and mediastinal lymphatic glands. — These were all 
distinctly enlarged, and on section showed white opaque spots 
(necrotic tubercles). 

Other lymphatic glands, — Visible tubercles were present in a 
renal lymphatic gland, in two of the mesenteric glands, in the 
right and left popliteal glands, and in one of the pre-pectoral 

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The following parts appeared healthy: heart, pleura, peri- 
toneum, and the axillary, pharyngeal, and pre-crural lymphatic 

Histology of the leaions.^^'RQTe, again, the tubercles had the 
usiial histology of such lesions in the ox. They were all under- 
going central necrosis and caseation. Giant-cells were present in 
most of them, but sparing in number. No calcification. Tubercle 
bacilli sparing in number. 

A most interesting feature of these cases is the contrast which 
they present to the generality of cases of tuberculosis in adult 
cattle. The most characteristic features of tuberculosis of the 
adult ox are (1) the frequency with which the pleura and peri- 
toneum are involved when the disease is at all extensive, and 
(2) the rarity of splenic lesions. As in other species, tubercles in 
the heart muscle are exceedingly rare, as are also lesions in the 
popliteal lymphatic glands. In both these congenital cases, how- 
ever, the tubercles were most numerous in the liver, and both cases 
had lesions in the spleen. 

The differences are partly explained by the fact that congenital 
tuberculosis is probably always generalised in the sense that it is 
due to blood infection, whereas generalised tuberculosis in this 
sense is relatively rare in the adult ox or cow. Furthermore, when 
the disease does become generalised in the adult animal the 
distribution of the lesions is entirely different from that seen in 
congenital cases. The tubercles which result from a blood infec- 
tion in the adult are always vastly more numerous in the lungs 
than in any other part, and the liver, spleen, kidneys, and body 
lymphatic glands may develop few or no tubercles. It is therefore 
quite erroneous to regard the presence of tubercles in the spleen 
as the most reliable evidence of generalisation in adult cattle, 
although this has* actually been done in the official regulations 
regarding the condemnation of tuberculous carcases in France. 

May 2nd, 1899. 

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4. Section showing a mycosis (? aspergillar) of lung of horse, 
{Card specimen,) 

By Alexander G. E. Foulerton. 

[With Plate Vin.] 

THE specimens show sections through the lung of a horse referred 
to by Prof. J. M^^Fadyean in the discussion on pseudo-tuber- 
culosis. The lungs presented macroscopically a number of small 
grey miliary nodules scattered throughout their substance. Each 
nodule contains a reniform mass of mycelium, surrounded by 
smaller round-celled infiltration. The mycelium in some places bas 
grown through the walls of the air-vesicles. In other places it 
appears to fill the lumen of small bronchioles. 

The mycelial filaments are closely packed in the central portion 
of the fungus mass, and separate somewhat towards the periphery 
in a radial fashion. The filaments are unevenly contoured, showing 
varicose swellings here and there ; they divide dichotomously in the 
peripheral portion of the mass, and some of their terminal branches 
are slightly bulbous at the extremity. No absolute indication of 
fructification can be seen, but the bulbous terminal extremities 
recall the appearance of the abortive attempts at the formation of 
a spore-bearing head, devoid of sterigmata or spores, observed 
when Aspergillvs fumigatus is grown under certain conditions in an 
atmosphere free from oxygen. The mycelium is stained by the ordi- 
nary basic aniline dyes, the peripheral portion of which takes the dye 
more deeply than does the closely packed central portion. Treated 
with Ehrlich's tri-acid solution the filaments stain a faint bluish- 
green colour. The whole mass of mycelium stains deeply with 
Ehrlich's hsematoxylin solution, and retains the gentian violet stain 
when treated according to Gram's method. 

Microscopically the appearance of the fungus closely resembles 
that seen in known cases of natural aspergillar infection, and also 
that resulting in guinea-pigs and rabbits after experimental intra- 
venous inoculation with spore-bearing cultures of Aspergilhis 
fximigatus, February 21g<, 1899. 

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Illustrating Mr. Alexander G. E. Poulertoa's paper on Mycosis 
(? Aspergillar) of Lung of Horse. (Page 272.) 

Fig. 1. — Stained with hsmatoxyliii. x 40. 
Fig. 2. — Stained with hsematox3liu. x 75. 

(Photographs by Mr. Barnard.) 

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rA^^ %: 


* '''; 



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• ■' i JN OV I'LATE Yfll, 

'^i '. . :v.Lti(i T G. R, F I'.u'toirs |''{<''i' on Mycosis 

■ ' . / oi I/ii'ir ')i H -:>.■. 


I ... U,--"*** till x'l -vitli ii:i '., iio>; 111.. . ,' ). 

'"' .;'-.;. .. l.\ Mr l5ii! ..i< 

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Path. Soc. Trans. Vol. L. Pl. VIII. 

Fig. 1. 

Fi|. 2. 

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5. Blackwater or hismoglobinuric fever. 
By W. H. Crosse and W. C. C. Pakbs. 

CONSIDERABLE attention has recently been called to blackwater 
fever, particularly by the assertion of Koch that it is really a 
form of quinism, or is produced by that drug. 

The account of a case which has occurred ia England and which 
we have had the opportunity of investigating is, therefore, we ven- 
ture to think, not without interest. 

Before referring to the case we should like to give a brief account 
of the disease in general. 

The fever occurs chiefly in tropical Africa among young Euro- 
peans. Its incidence among the natives is usually very small ; 
there is said to have been, however, an epidemic among them 
recently in the Cameroons. F. Plehn distinctly states that the fever 
does attack negroes in the Cameroons, but it has never occurred on 
the lower Niger, at least to our knowledge. 

It attacks only those who have suffered previously from malarial 
fevers, and who have, from various causes, become debilitated and 
run down. It usually comes on during the course of what appears 
to be an ordinary malarious attack, and some special exciting cause 
such as exposure to a chill or to the sun is generally to be noted. 
Plehn says that it may replace an ordinary attack of malaria. 

The mortality is usually great for reasons which will be explained 

An account of this disease is given in * Notes on Malarial 
Fevers,' by one of us, and also in an introductory address read 
before the Physical Society at Q-uy's Hospital on October 3rd, 
1898. The leading symptoms are : — (1) fever, (2) jaundice, (3) 
hsemoglobinuria, (4) nausea and vomiting (often green vomit) . 

In November of this year one of us (W. H. C.) was called in 
consultation with Dr. Wooldridge, of Camberley, to whom we are 
indebted for notes of the case, and Brigade- Surgeon Lieut.-Col. A. 
Clarke, to see a young officer who had recently returned to England 
after having served in Nigeria for fourteen months : the patient 
had had many attacks of malaria, dysentery three times, and was 
suffering from chronic dysentery on his arrival in England about 
the middle of November ; his last attack of malaria occurred at 
Q-rand Canary nine days previously. He arrived in England in a 


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somewhat debilitated condition. Six days later, though feeling 
somewhat unwell, he joined his brother officers at mess. Duriog 
mess he felt decidedly chilly, on the following day he had a rigor 
and went to bed. The next day, November 27th, he was noticed 
to be jaundiced, he had a severe rigor (the temperature rising to 
106°), his urine about noon became porter-like, and he began to 

The urine was examined by Dr. Wooldridge, who found a quantity 
of albumen, but was unable to detect more than one or two red 
discs in it. 

When seen by one of us the patient was lying in bed, pinched, 
jaundiced, and very debilitated ; his tongue was broad and flabby ; 
he suffered from constant nausea and vomited occasionally, the 
vomited matter being of a bright green colour ; the urine, which 
had been porter-like, had already (the third day of hsemoglobinuria 
and the fifth day of fever) b^un to clear. 

Sulphate of quinine and bicarbonate of soda were given by the 
mouth, and retained; the patient began to feel better almost at 

A specimen of urine and some blood films were obtained. The 
urine (collected on the third day of the hsemoglobinuria) had the 
appearance which is commonly described as ** smoky." Albu- 
men was present to the extent of rather more than one part per 

Sug ar and bile pigment were both absent. There was a faint 
band of hsemoglobin, but none of urobilin. The microscopic exa- 
mination showed a few red blood-discs, a very distinct increase in 
the leucocytes, a large number of granular casts and renal epi- 
thelial cells. Many of the casts contained brownish granules as of 

No crystals of any kind could be found. As it was impossible 
under the circumstances to examine the fresh blood, blood films 
were made. We stained and examined three. There was, we 
thought, no increase in the number of leucocytes after allowing 
for the aneemia. On the three slides nine parasites were found. 
The hfiematozoa were about a quarter the size of the red discs con- 
taining them. None of them contained any pigment. One was 
definitely ring-shaped. The red discs were not enlarged. No 
crescents could be found. 

The size of the parasites and the absence of pigment eliminated 

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the quartan parasite, and tlie absence of any increase in size of the 
discs almost eliminates the tertian one. On tbe whole, we thought 
the hsematozoa resembled those described as the malignant para- 
sites, but, as we have only been fortunate enough to examine the 
blood of one such case, our knowledge is nearly limited to de- 

After five days' improvement tbe patient had a slight i*elapse, a 
return of high temperature, and a single recurrence of smoky 
urine ; quinine was continued. 

Tbe urine was examined and was found to contain albumen, 
though in smaller quantities than on the previous occasion. Sugar 
and bile pigment were botb again absent. Haemoglobin was present, 
but again there was no urobilin band. 

Tbe microscope revealed a very few red discs, a slight increase 
in leucocytes, and a few granular casts and renal epithelium. This 
was a marked improvement on the previous specimen. 

Three days after the relapse blood films were again examined. 
No parasites could be found in any of the films, eitber intra- 
corpuscular or crescents. There was a marked decrease of the 
red discs, and in addition a definite leucocytosis ; several nucleated 
red discs were found. Since the relapse the patient has improved, 
quinine having been administered all the time. 

The important feature about this case is that the patient had 
several attacks of malaria in Africa, but his first attack of black- 
water fever occurred in England. 

As to the causation of this case of fever there appear to be 
three possibilities, each of which has been suggested as a cause 
for the disease. 

Firstly, the disease may be unconnected with either malaria or 

Secondly, it may have been produced by quinine. 

Thirdly, it may be directly connected witb the malaria. 

If the first contingency is correct it must follow that the latent 
period may extend to upwards of a month — tbe interval which 
elapsed between tbe patient leaving Africa and his illness, or tbat 
the disease may be acquired in England. These alternatives are, 
we think, botb untenable. 

That the disease was caused by quinine we think most unlikely, 
for the patient only took, and did not retain, five grains of quinine 
before the bsamoglobinuria developed. During the subsidence of the 

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hsemoglobiDuria quinine was given freely, much to the benefit of 
the patient. It is true that during the administration of quinine 
a slight relapse occurred, but in consequence of the relapse the 
quinine was materially increased. Since then the patient has 
continued to improve, and there has been no i-ecurrence of the 

Plehn says that he thinks that quinine, if given during the con* 
valescence from malaria of blackwater fever, causes, or is likely to 
cause, a destruction of the red discs and consequent heemo* 
globinuria. Koch has gone further, and said that the treatment 
of blackwater fever by quinine must cease. On the Niger, where 
one of us (W. H. C.) was stationed for nine years, we are con- 
vinced that in the majority of fatal cases of this disease, either 
the patient does not get sufficient quinine, or if he gets it does 
not retain it owing to the persistent vomiting, or the patient when 
first seen has ursemic coma or is actually dying. 

Dr. MofEatt, P.M.O. of the Uganda Protectorate, has publicly 
stated that most of his cases of blackwater fever which recovered 
were treated with heroic doses of quinine. 

We think the evidence against the quinine theory shown by our 
case is absolute. The attack came on whe n the patient had not 
had any quinine, the patient improved when quinine was given, 
and after the slight relapse he was much benefited by a consider- 
able increase in the amount of this drug given hypodermically. 
We think that the third alternative, that it is directly connected 
with malaria, is the correct one. 

As far as we know, blackwater fever occurs only in patients 
resident in, or who have resided in, the malarious tropical countries. 
A patient has always sufEered from malaria, generally many times, 
before he acquires his first attack of blackwater fever. Those who 
from any cause do not get malaria do not get blackwater fever. 

The usual incidence of blackwater fever is during the second 
and third years of residence in the malarious districts of tropical 
Africa, that is, we should suggest, when the patient is run down 
from several attacks of malaria, and before he is partially 

As we have already pointed out, the fever almost, if not quite, 
invariably supervenes upon an attack of malaria during which the 
patient has either not been able to lie up or has been exposed to 
cold or the sun. Plehn says that an attack of blackwater fever may 

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replace an ordinary attack of malaria, and lie mak^s the very 
significant statement, " Whether in any individual case an attack 
of blackwater fever occurs instead of a simple malaria (infection 
with the African malaria being presupposed) depends upon the 
time of the year, the situation of the residence, and the disposition 
of the patient." In our case we have found heematozoa, and they 
have been also found by other observers. 

Plehu states that hsematozoa are constantly present in the 
peripheral blood during the first day or two, but that they 
disappear from it after the second day. He also points out that 
the hsematozoon, while probably being a distinct African species, 
resembles rather that described as malignant by the Italians than 
the ordinary quartan or tertian varieties, and he goes on to say 
that the parasite found in blackwater fever differs in no way from 
that found in the ordinary malaria endemic in theCameroons. 

We think, therefore, that there can be no doubt that the disease 
has some definite and close connection with a hsBmatozoon. 

There appear to be two alternatives left. The first is that there 
is a special hsematozoon which causes this disease. This is not 
impossible, because we know that there are other hsamatozoa than 
those which cause the ordinary European malaria, of which there 
are three well-differentiated species. Texas cattle fever and tsetse 
fly disease are both hsematozoic, the parasite of the former being 
singularly like the malignant malarial parasite; this disease, as 
has been pointed out by Celli and Santori, is cured by large doses 
of quinine, and hsemoglobinuria is a not uncommon symptom of 
severe attacks.^ 

The second, tbat the disease is really a symptom in ordinary 
tropical African malaria, bearing a similar relationship to that 
disease that hyperpyrexia does to rheumatic fever. The analogy 
to this symptom is made still closer when one remembers that the 
hyperpyrexia of rheumatic fever is not influenced by salicylates or 
alkalifs, but must be treated separately. It seems to us that it is 
as justifiable to say that salicylates cause the hyperpyrexia, and 
therefore should not be administered during the continuance of 
that symptom, as that blactwater fever is caused by quinine. 

What we maintain, therefore, is that blackwater fever is to 
malaria what hyperpyrexia is to rheumatic fever. That quinine 

* The evidence of Plehn, however, as to the identity of the parasite with that 
of ordinnry African fever is against this supposition. 

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should be administered for the malaria, but that the hsemo- 
globinuric fever should be treated as a special and extra symptom 
in a manner analogous to the treatment of hyperpyrexia occurring 
during the course of rheumatic fever. We are not altogether 
satisfied that heroic doses of quinine need be administered, but 
we think that the drug should be administered subcutaneously in 
order to make certain that the patient retains it. 

While this paper was in progress, Dr. F. P. Mackie published in 
the ' Lancet ' of December 3rd, ** Notes on a Case of Blackwater 

We note that, having found the parasites in the stained films, 
he was unable to find them in the fresh specimens ; he does not 
even mention that the extra-corpuscular bodies which were so 
numerous in the stained preparations were seen. All who have 
worked at the subject of malaria say how much easier it is to find 
the parasites in the fresh specimens. 

The *• considerable number of faded or phantom-like red cells ** 
of which he speaks, may easily be seen in normal blood if the film 
has not been properly fixed. 

He was certainly fortunate to see ** a rosette sliaped organism 
which had evidently just broken up" in the peripheral blood 
twenty-four hours after the last rigor, and we would suggest that 
" the faintly stained extra-corpuscular bodies, mostly in groups of 
two and three " were merely blood platelets, which can be easily 
demonstrated in anaemic, or even normal blood. 

Notwithstanding the assertion that the actively motile 
organisms found after two days in the blood diluted with normal 
saline were not bacilli because they were spherical, we think that 
they might have been small oval bacilli. If they were really 
flagellated forms, the growth of the hsematozoon outside the body 
has been demonstrated. We fail to see why the addition of 
normal saline to the blood should have prevented him from 
obtaining permanent specimens; it is quite a common practice 
when examining for bacteria to dilute blood with sterile normal 
saline solution, in order that it may be spread in a more even 

We observe that torulse were found in the urine, but it is quite 
a usual thing to find them in urine which has been exposed to the 
air ; in fact, it is more usual to find torulee than the common yeast 
plant or any other true saccharoniyces. 

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Path. Soc. Trans. Vol. L. Pl. IX. 

FIfr 1. 

Fig. 2. 

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[»!• M h'li'^i'ioN OF IM. * i \ 


I "■;■ 

Kia. 1.— si) w- t' tiic :h I '71 '-I ■■ , . ^ 

• ■ »r:i"il iiu;u in bl'M> 1. 'J i. f.. ' 
t^ tl-i'ii I »«^ in t* c j.'n (• , »a'i itniti < » 
^u't'l ill*.) ifjhir Jini^rlar i rjux aiui i 
[i »'.iitH ol m1 't'H tiipy ai( ;..:'--' »i ii in.v 

KiG. 2.--^t owi.i/ t'-" .1. .;on . f Die i ' 
tlio i>i'-'Hl •)! a h'Ul i.'TiU t, I i'i,* 'ill 
'mLo isl.r '1' of v.ii'iou}* s./,"-* n;ul irrrv . 

* • urptntlei* held !i* !trl\ t\'Ur i !■ i.*. 

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f A- I s--. . ; .• \^•^ '/..■ i 

M m-' 

...#>:•-. .^ 

^'^ ; -.^ 

■ v.. 

v.. T 



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Illustrating Mr. S. G-. Sbattock's paper on Chromocjte 
Clumping. (Page 279.) 

Fig. 1. — Showing the action of pneumonic blood-serum upon normal human 
blood. Hanging drop made by admixing one loop of the scrum with one loop 
of normal human blood. The effect was immediate, and was denoted to the 
naked eye in the coarse granularity of the drop. The chromocytes are aggre- 
gated into long irregular rouleaux and produce a very coarse mesh, at the nodal 
points of which they are massed in irregular clusters or clumps. 

Fio. 2. — Showing the action of the blood-seram in acute rheumatism upon 
the blood of a leukssmic patient. The chromocytes at once became aggregated 
into islands of various sizes and irregular form. The elements between the 
chromocyte clumps are all leucocytes; these remained quite unaffected. The 
white corpuscles held nearly fifteen times the normal proportion to the red. 

(Photographs from drawings by Mr. G. T. Gwilliam.) 

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Lastly, we feel convinced that the case is unique in that the 
presence of granular casts is demonstrated in a urine which con. 
tained no albumen. December 20th, 1898. 

6. Chromocyte clumping in acute pneumonia and certain other 
diseases^ and the significance of the buffy coat in the shed 

By Samuel G. Shattock. 
[With Plate IX.] 

As a factor in the production of the buff j coat in the coagulation 
of normal blood, the rouleaux-formation of the red discs or 
chromocytes has come, at the present time, to be almost completely 
ignored, the phenomenon being ascribed solely to retardation in 
the coagulation rate. The coagulating time of cat's blood varies 
between three and eight minutes, the former being that at which it 
takes place at the body temperature, the latter at a room tempera- 
ture of 18° C. (Gregor Brodie) ; that of horse's blood is stated 
(after Nasse) to be from five to thirteen minutes. No buffy coat is 
formed in the first, a thick oae is formed in the second. Coagula- 
tion, as is well known, may be delayed by cold. What results if 
the coagulation of the two is retarded for an equal period ? The 
observation can be carried out simply enough by receiving the 
blood directly from the cat's carotid (from a transverse hemisection 
made with scissors) into a narrow flat-bottomed tube, say half an 
inch in diameter, and at once immersing the tube into a vessel of 
iced water. At the expiration of fifteen minutes there will be 
above the red mass a thin layer of perfectly clear plasma, which 
will attain a depth of 2 mm. in a column -of blood measuring 35 mm., 
i. e, 5*7 per cent. 

The blood is full of surprises. I had imagined that the influence 
of rouleaux-formation iu the production of the buffy coat might be 
tested in this simple manner. To my astonishment, I found that if 
horse blood is similarly iced, although coagulation may be retarded, 
the subsidence of the red mass and the consequent appearance of 
supernatant plasma instead of being increased is almost completely 
inhibited ; under such circumstances no more plasma appears than 
in the case of the cat, the amount in either being quite insignificant. 

July 10th, 1899. — Prom a healthy horse (previously tested by 

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Dr. Cartwrigbt Wood with mallein and tuberculiu, and about to 
be used for procuring serum for the preparation of culture media) 
blood was received from a cannula in the jugular vein into a 
flat- bottomed tube, half an inch in diameter, the tube being imme- 
diately placed in iced water. After twenty minutes (no clotting 
having ensued) there were but 3 mm. of supernatant plasma in a 
column of blood 36 mm. in height, i, e. 8*3 per cent. (In other 
instances still less has appeared in the same period.) 

I now removed the tube from the iced water : subsidence of the 
red mass quickly progressed ; within eight minutes the upper half 
of the whole column consisted of clear plasma, and the amount 
increased before coagulation took place, until it stood at twenty 
parts in thirty-six, i. e, 55*5 per cent. 

The striking effect of cold in inhibiting the subsidence of the red 
corpuscles (a fact which has apparently escaped the notice of phy- 
siologists) will best appear from the graphic representations of 
another observation. 

August 1st, 1899. — A horse, which had been three weeks an 
in-patient at the Brown Institution for a sprain of the shoulder, in 
the treatment of which a large blister had been applied nineteen 
days previously over the part, no remains of the therapeutic lesion 
now persisting. Into a narrow test-tube 5 mm. in diameter, I 
received directly from the jugular vein without intervening cannula 
or tube, blood to a height of 46 mm. 

At the expiration of five minutes there was a supernatant layer 
of clear plasma 2 mm. in depth. 

10 minutes . . . .12 mm. in depth. 

15 „ .... 23 

20 „ .... 24 

25 „ .... 25 „ 

By this time clotting had ensued. This gives a proportion of 
plasma equal to 54 per cent. After cleansing the same tube I at 
once received from the same jugular of the same horse a column 
of 50 mm., the tube in this case being kept in iced water before, 
during, and after the receipt of the blood. At the end of five 
minutes the clear plasma measured 1 mm. in depth. 

10 minutes .... 1 mm. in depth. 

15 „ .... 2 

20 „ .... 2 

25 „ .... 2 

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No clotting had ensued, as seen by tilting the tube in the glass 
of iced water, when not only the highest limit of the column cor- 
respondingly altered its level to maintain the horizontal, but the 
upper limit of the red mass did precisely the same. On removing 
the tube from the iced water after thirty minutes subsidence of the 
red corpuscles rapidly commenced, but coagulation occurred after 
an ill-defined 7 mm. of plasma had appeared. 

The percentage of clear plasma in the uncoagulated iced blood 
was but 4 as contrasted with 54*3. 

Fig. 21. 

The figures show the effect of cold in preventing the suhtidence 
of the red corpnsclei in horse blood. In each tube the blood was 
allowed to stand twenty-five minutes, and was still fluid, a. At the 
room temperature. B. In iced water. The black represents the red 
mass ; the upper line, the higher level of the clear plasma. The actual 
amount of blood differed slightly in the two observations, but for com- 
parison the proportions have been calculated in equal heights. The 
level of the fluid is represented, for simplicity, not concave but straight 
(Natural size.) 

In cat's blood a similar observation made in such an iced tube 
showed at the end of twenty minutes (no coagulation having 

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occurred) 2*75 mm. of plasma in a column of 55 mm., t. e, a pro- 
portion of 5 per cent., or practically the same as in the preceding 
observation* on the blood of the horse. 

This method of retarding coagulation being therefore unavail- 
able for testing the part taken by rouleaux-formation in the pro- 
duction of the buffy coat, I had recourse to the use of sodium 
citrate, which, like potassium oxalate, inhibits coagulation by 
combining with and rendering inert the lime, the presence of 
which in normal blood is one of the essential factors concerned in 

Into a 10 c.c. measure containing '25 c.c. of a 10 per cent, 
solution of sodium citrate blood was received from the carotid 
artery of a cat, rolled to ensure mixture, and allowed to stand. 
For the first ten minutes no subsidence of red corpuscles was dis- 
cernible ; in fifteen minutes a layer of plasma 3 mm. in depth had 
appeared in a column of 57 mm. ; in thirty minutes the layer was 
7 mm., i. e, 12'2 per cent. Coagulation was completely inhibited. 

A similar experiment made with normal horse blood showed 
within fifteen minutes a layer of plasma 37 mm. in depth in a 
column of 56 mm. ; and in thirty minutes the layer was 39 mm. ; 
i,e. 69*6 per cent, as contrasted with 12*2 per cent, in the cat. 
Better still, as introducing less of what is unnatural, is the ob- 
servation of Lord Lister's that in "whipped" blood from the 
horse the amount of subsidence of the red corpuscles in the serum 
is notably greater than, c. g,, in the cow. 

The highly pronounced rouleaux-formation in the blood of the 
horse has long been known, and to this has been ascribed in past 
times the production of the buffy coat, the element of time having 
been put into the background as completely as that of rouleaux- 
formation has now come to be. If one examine blood in the hang- 
ing drop (the best method, since fallacies arising from concentra- 
tion of the serum are obviated, and the rouleaux may be studied 
just as they form, unmodified by compression) a notable difference 
appears between that of the cat, e, g., and that of the horse. 

The hanging drop of blood from a healthy horse shows on 
immediate microscopic examination a highly pronounced rouleaux- 
formation, associated with a widely meshed and knotted field in 
which there are vacant spaces traversing, it may be, the entire 
thickness of the drop ; the appearance holds throughout the pre- 
paration, both, i. e., at the thinner periphery and in the central 

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parts. If one loop of horse blood is mixed with one loop of salt 
solution, the picture presents the same features; the rouleaux 
retain conspicuous length and form a coarse knotty mesh, the 
spaces of which are more vacant owing to the increased volume of 
the fluid due to the dilution. 

The hanging drop of normal cat's or of human blood presents a 
more closely meshed field, with rouleaux correspondingly shorter ; 
and in either case the effect of dilution is different from that in 
the horse. If one loop of cat's blood be mixed with one loop of 
salt solution, the rouleaux-formation is largely inhibited, the piles 
of chromocytes being quite short, and the mesh very imperfect or 
discontinuous, whilst at the same time it is finer in correspondence 
with the shortness of the rouleaux. 

When untreated human blood is examined in the hanging drop, 
and compared with the mixture of an equal proportion of salt 
solution, the action of the latter is seen to almost completely in- 
hibit the formation of rouleaux; the field is uniformly covered, 
without lacunae, the rouleaux being very short and the mesh they 
produce very close, so close in places as to be quite wanting. 

This result may hypothetical ly be attributed to the dilution of 
an a^lutinating substance normally present in the blood ; and it 
may, moreover, be assumed that in the horse the amount of this 
substance considerably exceeds that in the human subject, seeing 
that it will withstand dilution to a notably larger extent before 
losing its action upon the chromocvtes. 

I may now pass on to a further observation which I was induced 
to make for the purpose of seeing whether the serum of horse 
blood would exaggerate the rouleaux-formation in pther blood 
than that of the horse. Its influence in this respect upon human 
blood is readily tested in the hanging drop, by placing a loop of 
serum on a cover-glass and mixing with this a loop of blood 
freshly drawn from a puncture of the finger made near the root of 
the nail. 

The microscopic examination (best carried out in all cases with 
'} obj.) shows an increased rouleaux-formation with the produc- 
tion of a coarsely meshed field, and nodal masses or clumps of 
chromocjtes in the course of the net, the chromocytes appearing 
as if aiTanged in knotted strings; not only are the rouleaux 
longer, but they construct a wider net with vacant intervals, the 
whole picture contrasting with a preparation of normal human 

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blood admixed with an equal proportion of nonnal human blood- 
serum. If the latter control is made, viz. that of mixing one loop 
of normal buman serum (from blood collected in a pipette) with 
one loop of normal human blood, no such result follows; the 
hanging drop of such a mixture is not appreciably different from 
a hanging drop of normal human blood; the rouleaux maintain 
the same moderate length and produce a uniform and compara- 
tiTelj close net, but markedly less close than that seen in the drop 
prepared with one loop of normal human blood and one loop of 
salt solution. 

This observation shows that the rouleaux-fonnation in the blood 
of the horse is not to be ascribed solely to qualities in the red 
corpuscles, but that it is due, also, to some property of the serum. 
And, adopting the t.erminology in use with regard to the bacterial 
clumping which ensues under the action of specifically immunised 
sera, it may be formulated that rouleaux- formation is a pheno- 
menon of agglutination arising from the same cause as that which 
obtains in the case of bacteiial infections, and that tbe amount 
of agglutinating substance normally present varies in different 
animals. As confirming this hypothesis, if we add one loop of 
normal horse serum to one loop of a twenty-four hours' incubated 
broth culture of living typhoid bacilli (from which any clumps 
present have been first removed by filtration through a double 
cone of Schleicher's paper, and the examination of which, so 
filtered, shows active mobility and no clumps), notable agglutina- 
tion or clumping immediately ensues, and witbin the half-hour 
limit is so complete tbat every field is full of bacillary islands. 
What dilution will the serum withstand ? This varies somewhat 
with different samples: 1 in 20 may or may not abolish the 
reaction ; 1 in 50 will. In the study of such hanging drops there 
is a possible source of fallacy worth pointing out ; the clumps may 
subside in the drop so as to be discoverable only when its lowest 
or deep side is brought into focus, the rest of the fluid, it may be, 
presenting only discrete and mobile bacilli ; in control preparations 
I have noticed this, though the broth culture has been carefully 
filtered ; or, if present elsewhere, the islands may be most numerous 
in the under side of the drop. The notes of the observations 
themselves need not be detailed ; they were carried out with 
twenty- four hours' incubated broth cultures of the bacillus, the 
culture being filtered immediately before use through Schleicher's 

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paper ; the time limit adopted was half an hour ; control prepara- 
tions were invariably made, the examination of these being equally 
prolonged.^ In one case the agglutination remained well pro- 
nounced under a dilution of 1 : 50. At this dilution eveiy field 
presented many clumps of medium size, whilst the control prepara- 
tion made at the same time exhibited no clumps whatever, not 
even'at the deepest side, but was full throughout of actively moving 
bacilli. This result led me to suspect that the horse (an in- 
patient at the Brown Institution, for a sprained leg) may have 
been at some time used for the raising of antityphoid serum 
and afterwards sold for work; the owner had bought it a 
few weeks previously at a sale, but no further history could be 

I was independently led to try and find the action of normal 
horse serum on typhoid cultures by reason of the highly pro- 
nounced agglutination of the chromocytes which naturally occurs 
in the blood of this animal, and which the serum induces in 
human blood ; though the fact had been previously noticed by 
Johnson and MacTaggart. The same factor in the serum which 
leads to the one brings about the other. 

There is a further likeness in the two phenomena which I may 
next refer to. The action of cold in inhibiting the subsidence of 
the red corpuscles in horse or other blood I have already shown ; 
and I imagine that the result is due not to change in specific 
gravity but to an inhibiting of rouleaux-formation, for the reason 
that cold acts in a precisely analogous manner upon u mixture of 
typhoid culture and normal horse serum. To study this micro- 
scopically a cold stage would be necessary, but the effect is 
readily observable in the gross. Into a flat-bottomed glass 
tube, about half an inch in diameter, 2 c.c. of an incubating 
broth culture of typhoid of twenty-four hours' growth were 
poured, the vessel being then placed in the incubator ; and into 
a similar tube 1 c.c. of normal serum from a horse previously 
tested with malleiu and tuberculin. After the serum had been 

* Some of the horses had been carefully tested with mallein and tubercnlin by 
Dr. Cartwright Wood at the Tooting horse farm, and by Dr. Dean at the Sudbury 
one; others were in-patients at the Brown Institution for simple ii\juries; and I 
may here acknowledge the kindness with which material and help were placed at 
my disposal by Dr. Gregor Brodie, Dr. Cartwright Wood, Dr. Dean, and Prof » 
Bose Bradford. 

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warmed in the incubator it was emptied into the culture, the two 
being mixed with a warm rod and the tube replaced in the incu- 

To compare : 2 c.c. of the same broth culture in a similar glass 
tube were cooled in iced water and to these was added 1 c.c. of the 
same normal horse-serum, previously also iced ; mixing was carried 
out with an iced rod and the vessel afterwards kept immersed in 
iced water. 

The typhoid culture itself was not filtered, and was to the naked 
eye turbid without visible granularity. I first carefully observed 
that the icing of the typhoid culture for fifteen minutes before 
adding the iced serum produced no result visible to the eye. 
What followed ? The iced mixture remained uniformly turbid 
even when viewed with a pocket lens for the entire half-hour 
during which it was under observation. The incubated tube in 
the same time had become throughout coarsely granular to the 
unaided eye. 

After fifty minutes, the iced tube remaining free of granularity, 
I removed it from the bath of iced water, and held it in the 
palm of my warm hand ; within the space of five minutes it grew 
finely granular, and on transferring it to warm water the granu- 
larity became very pronounced during the next five minutes. 
Subsidence then proceeded, the flat bottom of the tube being 
covered with a sedimentary layer, and an upper zone of half a 
centimetre depth becoming cleared after the lapse of about twenty 

In the mixture incubated throughout, after fifty minutes, the 
granular precipitate was collecting over the bottom of the tube ; 
the upper part of the fluid was clear. 

In another experiment with an iced mixture, no trace of granu- 
larity having arisen at the expiration of three quarters of an hour, 
I held the tube in a tumbler of warm water, and watched it with a 
pocket lens ; within five minutes an obvious granularity had arisen, 
and within fifteen minutes this was so coarse, as to be visible to the 
unaided eye. The actual descent of the bacillary clumps, however, 
does not proceed rapidly. In such mixtures whether iced or incu- 
bated, even after eighteen hours, when sedimentation is complete, 
a certain number of granides remain suspended. Sedimentation 
takes place more rapidly with a typhoid culture that has incubated 
for forty-eight hours, than with one of twenty-four. 

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Thus a mixluve of the same proportions kept at the room 
tenperature, though graDuIar throughout, showed do subsidence at 
the end of fifteen minutes ; in forty-five minutes, the granulaiity 
being coarser, sedimentation was in progress; after sixty minutes 
there was a sedimentaiy layer at the bottom of the tube, but the 
fluid was full of coarse granules in suspension; and no further 
t harge had occuried in seventy -five minutes. On the day following, 
the same broth culture, in the meanwhile incubating, was used for 
an exactly similar experiment. Obvious granularity arose within 
five minutes. In fifteen minutes sedimentation was in active 
progress, the fluid being more densely granular towards the bottom 
of the tube, over which an incomplete layer had formed ; in thirty 
minutes the deposit had much increased; in forty-five minutes, 
though the fluid was nowhere clear, most of the precipitate had 

The same difference has been observed in the agglutination 
induct d in typhoid cultures of twenty-four and forty-eight hours 
age by the action of typhoid serum. 

This result of cold may be provisionally explained by supposing 
that it inhibits or retards a process that is, whether in chromocyte 
or bacillary clumping, essentially chemical. 

Lord Lister prefaces his study " On the Early Stages of Inflam- 
mation " (* Philosophical Transactions,' 1858) with many observa- 
tions upon rouleaux- formation in normal blood. He remarks that 
the formation can have no dependence upon the coagulation of 
fibiin, since it is immediate, and occurs before coagulation. Again, 
in corrobation of this, "if a drop of blood is stirred with a needle 
while coagulation is taking place, so as to remove the whole of the 
fibrin, the corpuscles, which have been separated from one another 
by the agitation to which they have been subjected, aggregate 
again in the seium, in the same manner as they did at first, in the 
liquor sanguinis. " 

The formation of rouleaux is attributed by Lord Lister to a cer- 
tain, not very great degree of adhesiveness of the red corpuscles, and 
the particular arrangement of the corpuscles, to their discoid form, 
for " in the frog, although the same tendency to agglutination 
exists as in mammalia, yet as their biconvex form renders it 
mechanically impossible for them to be applied to one another 
throughout their entire circumference, they become arranged in 
groups of an irregular form." 

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Passing from these physiological considerations, I may re-state 
the observation made by Wharton Jones, that in the blood of 
inflammatory diseases, the rouleaux are formed more rapidly, and 
run into masses which have larger spaces between them. Two 
figures contrasting this with the rouleaux formation of normal 
blood are given by Sir James Paget in his * Lectures on Surgical 
Pathology ' (ed. 3, fig. 36). 

The thin clot outspread on the glass has in such diseases, as Sir 
James Paget states, the peculiar mottled pink and white appearance 
which John Hunter observed as one of the characters of inflam- 
matory blood. And the production of the buflFy coat in such blood 
was ascribed by Wharton Jones to this closer aggregation, and the 
more rapid subsidence therefrom resulting (* British and Foreign 
Medical Review,* October, 1842). This observer examined blood 
drawn in a case of peritonitis, in one of pericarditis, and in one of 
pneumonia ; in each a buffy coat formed, and a microscopic prepara- 
tion made from the blood whilst flowing showed an exaggerated 
rouleaux-formation. Wharton Jones states that this view of the 
production of the buffy coat in such diseases, was first propounded 
byNasse, and afterwards noticed by Rudolph, Wagner and Henle. 

Having arrived thus far, I may now record my own observations, 
which were made with the object of seeing whether the blood 
serum from patients suffering with acute pneumonia, erysipelas, or 
rheumatism had any result upon the rouleaux-formation of normal 
human blood. The blood serum \ised was in all eases obtained 
from blood received into pipettes, which were at once sealed in the 
flame, and kept in the dark for after use. 

If wo add one loop of the blood serum from a patient suffering 
from acute pneumonia to one loop of normal human blood, a 
highly remarkable result ensues in the hanging drop, and one that 
is strictly comparable to the result I have already described as 
happening when normal horse serum is added to normal human 
blood. The blood serum used in the first test was from a woman 
admitted to St. Thomas's Hospital January, 1899, and taken whilst 
the temperature was still high, and the physical signs of pneumonia 
were present. Four pipettes of blood were drawn on February 
2nd. On adding one loop of normal human blood to one loop of 
the pneumonic serum, an immediate result was obvious to the 
naked eye, the drop appearing as though it held a deep red precipi- 
tate in suspension. Under one-sixth objective, the chromocytes 

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were seen to have run together into long rouleaux, which formed a 
complete, very coarse network, not only at the thinner marginal 
part, but throughout the drop; at the nodal points the discs were 
clustered into large knotted masses. Even in the central thickest 
part of the drop, the net was so coarse and sharply defined, that 
the lacunae were quite empty, from the upper focus to the lower. 

The action of salt solution upon normal human blood (1:1) is, 
as already described, to almost abolish rouleaux formation and 
netting. What is the result if normal human blood-serum is 
added (1 : 1) to normal human blood ? 

In this control no appreciable difference ensues from the picture 
presented by normal human blood; the rouleaux maintain a 
moderate length, and construct a uniform and comparatively close 

In a second case the blood was drawn in pipettes on May 2nd, 
1899, from a well-pronounced case of acute pneumonia with a high 
temperature; the serum added to normal human blood (1:1) 
gave the same result. 

The blood-serum, however, stands very little dilution. If one 
loop of salt solution is mixed with one of the serum, and to one 
loop of the mixture is added one of normal blood, the typical 
picture no longer presents itself, the hanging drop not being 
appreciably different from that of normal blood. 

In none of their experiments have Dr. Washboum and Dr. Eyre 
ever obtained a clumping reaction upon the pneumococcus by means 
of the blood-serum of animals experimentally immunised. Being, 
therefore, anxious to see whether the serum of pneumonic blood 
taken from the human subject during life would have any specific 
action, I made a suspension of the diplococcus on a cover-glass in dis- 
tilled water,! and from this transferred a loop to a second cover-glass 
to study as a hanging drop. At the same time a second hanging drop 
was prepared by adding one loop of the pneumonic serum to one 
loop of the same suspension. For at least twenty minutes no differ, 
ence was noticeable in the two preparations, but some time within 
twenty and fifty minutes of their making well-marked clumping 
ensued throughout in the serum mixture, the bacterial islands 

1 The distilled water is for snch and similar purposes best prepared for imme. 
diate nse by allowing bteam from a beaker to condense on the under side of a capenle 
partly filled with cold water, and quickly inverting the latter so at to bring the 
under side uppermost. 


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being parted by large clear intervals, whereas the control pre- 
paration examined at the same period had undergone no change 
whatever. This admixture (1:1) is, of coarse, one of high 
strength, but that the result was specific was shown by treating 
one loop of a 24-hours incubated and filtered (through filter-paper) 
broth culture of typhoid with one loop of the same pneumonic 
serum. Though the examination was prolonged for forty minutes, 
no similar result ensued; the bacilli remained quite active in 
large numbers in every field, a very few minute clusters being all 
that appeared. 

I submit, then, that in the production of these results, the same 
cause, the same change in the serum, which leads to clumping of 
the pneumococci accounts for that of the chromocytes, and if the 
hypothesis of an increased amount of " agglutinating " substance 
meets the first, it may be extended to the second. The formation 
of a buffy coat in acute pneumonia and other bacterial diseases, in 
short, may be viewed as a Durham's reaction, the agglutination of 
the chromocytes leading to their more rapid subsidence, and the 
clearing of the upper part of the plasma. Or, more accurately, it 
may be compared with Widal's reaction, seeing that it is obtain- 
able during the period of infection. This interpretation of the 
phenomenon neither increases nor lessens the difficulty of ex- 
plaining the specificity of bacterial clumping. It is quite obvious 
that the mere increase of an agglutinating substance will not 
account alone for bacterial cohesion, otherwise the result would 
obtain indifferently in the case of any bacterial cultures. 

Some specific interaction between the bacilli of the culture and 
the blood-serum must be supposed, which brings the agglutination 
about ; the bacilli cannot behave passively under an increase of 
"agglutinin;'* some other, as yet, imperfectly known factor 
underlies the phenomenon. Such an increase, however, acting 
upon indifferent elements, such as the chromocytes appear to be» 
may lead to this abnormal cohesion and exaggerated rouleaux* 
formation, and in this way to the production of the buffy coat in 
bacterial diseases. 

I may next briefly note the results upon normal human blood 
of the blood-serum from cases of erysipelas, typhoid, and acute 

In erysipelas the same result ensues as I have previously described 
in acute pneumonia. The serum tested was from the blood of a 

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child with a temperature of 103** F., and in whom erysipelas arose 
at the site of a dischargmg tubercular lesion of the leg. The 
mixture of one loop of the serum with one loop of normal blood> 
was followed by an obvious macroscopic granularity in the hanging 
drop; and on microscopic examination there was seen to have 
resulted a widely meshed picture with empty spaces, and dense 
clusters of chromocytes on the threads of the net, i, e. clusters so 
dense as not to be resolvable into a meshwork, the whole being 
strikingly different from that obtained in the control hanging drop 
made at the same time by adding one loop of normal human blood 
to one loop of normal human blood-serum. 

Typhoid. — The result in this disease I have not found quite so 
pronounced as in either of the foregoing, though a positive and 
sufficiently obvious one ensues. The hanging drop of an equal 
admixture of typhoid blood-serum and normal human blood 
showed throughout, when compared with a control made with 
normal human serum and normal human blood, a rouleaux-forma- 
tion of exaggerated length and abnormally coarse mesh. 

Acute rheumatism.— 1 tested the action upon normal human 
blood, of the blood-serum from a man who had been ill twelve 
days with acute rheumatism, his temperature at the time the blood 
was drawn being 103° F., at which date there was also pericardial 
friction. Equal quantities in the hanging drop, gave nothing very 
striking on immediate examination, but the picture shortly grew 
quite characteristic, long rouleaux forming with wide meshes, and 
coarse clumps, the drop itself becoming notably granular to the 
naked eye. 

Not only does the reaction obtain during the period of infection, 
but it persists during that of convalescence ; for how long 1 am 
not able to state. 

On March 30th, 1899, blood was drawn into a pipette from a boy 
who had been admitted for acute rheumatism; the blood was 
drawn the day after the temperature had fallen to the normal. 

One loop of the serum added to one loop of normal human blood 
in a hanging drop gave immediately an obvious macroscopic granu- 
larity, and showed beneath the microscope an abnormally wide and 
irregular mesh of chromocytes with long rouleaux and large clumps 
of chromocytes in the course of the net. In this case I again 
tested the blood serum from blood drawn on the thirteenth day 
after the fall of the temperature to the normal. The same clumped 

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or knotted picture presented itself. These results show tha4i the 
change in the serum leading to the increased agglutination persists 
during convalescence as in the bacterial clumping obtainable in 
specific infective diseases. 

The blood-serum, however, as in the case of pneumonia, with- 
stands very little dilution. If the loop of rheumatic serum is 
diluted with four of distilled water, and one loop of such a mixture 
is added to one loop of normal human blood, it produces no such 
result. Even when one loop of serum is diluted with only one of 
distilled water, and one loop of the mixture is added to one loop 
of normal blood, the picture is very little modified from the 

Among the leucocytes no cohesion ensues. This can be seen in 
preparations of the kind described, where leucocytes may be 
observed lying in the lacunsd of the chromocy te mesh in all degrees 
of proximity without cohering. But it is most strikingly observ- 
able on treating leuksemic blood with, e. g,, rheumatic serum. In 
such circumstances the chromocytes immediately become agglu- 
tinated into widely separated islands unconnected with a mesh, 
of irregular form; the islands consist of rouleaux, but these 
are so compact as to leave no mesh or only one that is very 
close ; at the thinner marginal part of the drop in such a prepara- 
tion there may be well-marked rouleaux associated with minute 
clumps. The leucocytes, on the contrary, however large their 
numbers, remain quite unaffected. 

The serum used in this particular instance was from a man who 
had been twelve days ill with acute rheumatism, his temperature 
when the blood was drawn being 103° F., at which time, also, there 
was pericardial friction. 

The cohesion of the red corpuscles was held by Lord Lister (loc. 
cit., * Phil. Trans.,' 1858) to constitute an important element in the 
production of stasis in the vessels of an inflamed part. And I 
would conclude by asking how far bacterial clumping arisiiig 
during life may not be responsible for the determination of the 
lesions met with in the later stages of bacterial disease, i. e. at a 
time when this agglutination may be brought about by the change 
of the blood which arises in the natural course of the disease 
itself. The lodgment of such bacterial emboli during the earlier 
periods of infection would lead to progressive lesions ; whilst occur- 
ring later, such emboli, though for the time rendered harmless by 

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natural anti-toxinisatioD, miglit constitute latent sources of future 
local recrudescence. 

The difficulty of explaining the secondary affections in pyemia 
as due solely to vascular thrombosis and the transference of emboli 
from a primary focus is removed, if the circulating cocci may clump 
in any parts of the circulatory system, since they might as a result 
become implanted in situations having no correspondence with an 
anatomical distribution of vessels related to the seat of a primary 
vascular thrombus. In fact, given the infection, there is no reason 
why such bacterial embolism should not avail to cause suppurative 
lesions without the presence of any primary vascular thrombosis 
whatever. Fehruary 2nd, May 7ih, 1899. 

7. An account of some experiments upon the toxicity 
of normal urine. 

By W. P. Hbeeinoham, M.D., F.E.C.P. 

EVER since it became known that renal disease could produce 
death, the common, and until lately universal, belief ascribed 
this result to the retention of waste products. They were at first 
thought to be those excreted, later to be some modification of them 
produced by retention, and lastly to be some antecedent of them, 
such as the salts of carbamic acid. Of recent years, indeed, 
another theory has entered the field, whose supporters maintain 
that the cause of ursBmia is not the accumulation of waste products 
in the blood, but the perversion or loss of an internal renal secre- 
tion. The evidence brought forward in support of this is, however, 

Those who held the former, still the common view, have lain 
under the disadvantage that they have never been able to point to 
any special substance excreted in normal urine, to which could be 
attached the poisonous properties required to explain the symptoms, 
while at the same time the means of investigation were of necessity 
imperfect. For injection of urea or other substances separately, 
into the blood of an animal, is an experiment open to much error. 

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If we could first prove that the urine itself was poisODOUs, and 
could tben remove one by one all the substances it contains, leaving 
the rest each time unaltered, we should by thus changing one 
alone of the many factors concerned be using the method of differ- 
ence in its strict form, and should obtain the best form of evidence 
known to inductive inquiry. But this is not possible. Such an 
elimination, in which we should remove one " spilikin " out of the 
heap without touching the others, is chemically out of the question. 
On the other hand, in the separate injection of each constituent, we 
alter, not one alone of the many original factors, but all of them 
save one. 

Now the first part of the experiment, the injection of urine into 
the blood, was performed eighty years ago. The conclusion was 
then formed, and is held now, that the urine so injected causes 
death. Whether this injection reproduces the conditions of 
ursemia, is a question which may for the moment be left uncon- 
sidered, while we trace the curious fortunes of this research. 

In 1822, Vauquelin and Segalas ^ injected urine directly into the 
circulation, and stated that it caused death. But their experiments 
were rightly discredited. They were only two in number. The 
first was performed on a dog, from which apparently one kidney 
had been removed, and which had been bled immediately before. 
About 90 c.c. of urine were injected, and the animal died in ten 
minutes. The second animal died a fortnight after the injection 
with double pneumonia and sero-purulent pleurisy. There was 
probably septic infection at the time of the operation. No weights 
are gi^en, and no conclusions can be founded on these experiments. 

In the same volume Gaspard ^ states that he injected 1^ oz. of 
fresh human urine, into the jugular of a large dog without serious 
results. He cites Bichat and Courten as having already done the 
same. This was apparently before 1812, and I do not know where 
their performances are recorded. Frerichs * many times injected 20 
to 40 grms. of filtered human urine into dogs and cats without ill 

Thus the opinion was formed that the urine was innocuous when 
injected into the blood, and in Cohnheim's * Lectures ' (1877), as 
well as in Voit's article on ** Urgemia, '* * this is taken for granted. 

^ ' Magendie's Joarn. de Physiol./ 1822, tome ii, p. 854. 
s Ibid., p. 34. 

» 'Die Bright'sche Nierenkrankheit,' 1851, S. 106. 
* * Ztschr. f. Biol.,' Mflnchen, 1868, Bd. iv, S. 142. 

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The fact was that the doses employed were much too small. But 
in 1881, Feltz and Eitter ^ published a long series of researches in 
which they demonstrated conclusively that the urine, whether 
canine or human, was toxic when injected into the blood of dogs, 
and, like many others, they yet found that the separate injection of 
its various organic constituents produced no serious symptoms. 
Thus they injected urea, urates, hippurates, creatin, creatinin and 
its salts, leucine, tyrosine, taurin, xanthine, hypoxanthine, and 
guanin, in far larger doses than could be contained in a fatal dose 
of urine, yet found no ill effects. After trying inconclusive experi-. 
ments with dialysis, they at last burnt off from the dry residue of 
evaporated urine all the organic constituents, and then found that 
the mineral salts were as toxic, or even more toxic than the original 
fluid. After experimenting with the various mineral salts con- 
tained in it, they concluded that the toxic effects are due to the 
salts of potassium which it contains, and to nothing else. 

At the same time and quite independently Astachewsky ^ reached 
the same conclusion. In 1883, Schiffer^ published experiments, 
the only useful outcome of which was the statement that, of urine 
freed from mineral salts, it required a litre, to a litre and a half, to 
kill a large rabbit. In these doses normal salt solution might well 
prove fatal. Some years later, Bouchard embodied the contents of 
several papers already contributed to the Socidte de Biologie and 
Academie des Sciences in his lectures on auto-intoxication. ^ He 
fully confirmed the fact of urinary toxicity, gave the average fatal 
dose of human urine as 60 c.c, and, while allowing that potash 
salts were to a considerable degree responsible for the result, claimed 
a share for every other constituent, and in especial for the organic 
extractives. Assuming these to give to the urine about one third 
of its poisonous total, he deduced therefrom an elaborate theory of 
auto-intoxication which will be discussed later. He worked with 

Albu ^ in the course of his work tried similar experiments, but 
found the results with rabbits very variable. 

1 * De rur^mie exp^rimentale,' Paris, 1881. 

s ' St. Petersb. med. Wochnschr./ 1881, No. 27. It is cited by Horbaczewski, 
' Wien. med. Jahrb.,' 1888, S. 889. I have not seen the original. 
» * Verbandl. d. Ver. f . innere Med.,* 1883-4, Jahrg. 3, S. 18. 
* Translated by C^ver, London, 1896. 
« ' Ueber die Anto^toxicationen des Intestinal-Tractus,' Berlin, 1895. 

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During the last three years I have been engaged in repeating 
Bouchard's experiments, and in 1898 Beck,^ who has been at the 
same task, brought out an important paper upon the subject, whose 
results will be given later. 

I have experimented with rabbits, since it is an easj and painless 
operation to inject into their large auricular vein. The fine 
syringe-needle is connected by tubing with a burette, and a steady 
flow is ensured by a hand air-pump, attached by a perforated cork 
to the burette. If the injection be too slow, interrupted, or irre- 
gular, excretion may so far interfere with the results as to render 
the experiment valueless. K it were possible, it would be best to 
vary the rate of injection inversely with the toxicity of the sample, 
that the fatal dose of the poison might always be placed in the 
circulation within a uniform time. But our ignorance of the fatal 
dose of each sample as it comes prevents this, and the next best is 
to keep the rate uniform for all the series. I have always^jected 
10 c.c. per minute. 

No aiuesthetic is necessary. The animal will often remain 
perfectly quiet throughout the operation. If it is wild, it can be 
held quiet; to fasten it down disturbs the rabbit, and thereby 
interferes with the natural evolution of the nervous symptoms. 
In registering the blood-pressure it is of course necessary to fasten 
the rabbit. 

The urine must be filtered clear. I neutralise it ; but in a few 
cases, whose results I could compare, urine was of the same toxicity 
when acid and when neutralised. The longest that I have kept it 
has been when collecting the excretion of twenty-four hours, that 
is about twenty-six hours from passing the first sample. I have 
sometimes warmed it to near the body heat, more often injected 
at the temperature of the room. When the injection is thus per- 
formed, the symptoms follow a fairly regular course. 

1. When about 20 c.c. have been injected the pupils b^n to 
contract, and the contraction usually increases till they are pin- 

2. The animal generally gets drowsy. Sometimes this effect is 
only slight, sometimes the eyes shut and the head bobs just as that 
of a man asleep in a chair. 

3. A sort of muscular twitch begins in the neck. It looks like a 

* 'Arch. f. d. ges. Physiol.,' Bonn, Bd. Ixxi, S. 660. 

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gulping movement. Eabbits do not vomit, but this may be a sort 
of retching. 

4. In many cases the bowels act, sometimes loosely. 

5. In many a little urine, up to 30 c.c, is passed ; rarely the 
flow is more copious. 

6. The respiration, either with or without previous acceleration, 
gradually falls in rate ; when it falls below 100 there is some em- 
barrassment of expiration. This increases and the rate of breathing 
falls, till death. 

7. Beck's observations on the circulation will be mentioned 
later. One cannot count the pulse or auscult the heart reliably. 

8. As the breathing becomes difficult, the rabbit wakes up and 
becomes a little restless. A few spasmodic movements of the head 
usually precede a fit of convulsions, which, beginning with clonic 
movements of the limbs, quickly end in strong opisthotonos. The 
animal generally dies in the first fit, but sometimes respiration 
begins again, and a second, third, or even more occur before death. 
Fibrillar tremor of the skin may occtir at almost any time during 
the injection, or may be absent. 

9. In opisthotonos the eye protrudes, and the pupil often dilates. 
After death — . 

10. If the temperature be taken directly, it will be found to have 
faUen considerably. 

11. If the body be at once opened, the heart will be found uni- 
versally dilated and full of fluid blood. Flickering contraction 
occurs here and there, and a touch will produce it. If the exami- 
nation be postponed for half an hour the heart is found contracted. 
The brain and lungs^are natural, the liver full of blood, the kidneys 
and spleen natural. 

Beck made the following important observations on the blood- 
pressure and pulse during the injection : 

1. The respiration quickens gradually up to a certain point as 
the urine is injected, and then begins to get slower. 

2. Slow injection has little effect on the blood-pressure or 

3. If more rapid the pressure falls and the pulse slows. These 
effects soon w^ar off, if the injection be stopped or slowed, and can 
be reproduced by again quickening it. 

4. They are then followed by restlessness, spasms, and sudden 
stoppage of respiration. 

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5. All these symptoms appear also if the injection be slow, but 
it needs much larger doses. The blood-pressure falls to zero 
before death* Eespiration stops altogether a little before the last 
heart- beats, but artificial respiration does not alter the course of 
events. Section of the vagi makes no difference, so that the heart 
is affected peripherally. Similar symptoms follow the injection 
of a solution of the mineral ashes of urine. Similar symptoms 
follow the injection of an 0*4 per cent, solution of potassium 

That the potash salts were one of the chief poisonous constituents 
was to be presumed. Their known toxic qualities and the toxic 
nature of the urinary ash was enough to prove that much. There 
arose, however, the question whether there was another poison 
aiding them. Bouchard, introducing the accuracy of mathematics 
into a subject which is wholly unsuited to it, endeavoured to 
assign to each constituent of the urine a partial toxicity. Thus, 
reckoning that the twenty-four hours' urine was capable of killing 
461 grms. of living animal, he calculated that — 

Potash killed 217 grms. 

Soda killed 80 „ 

Calcinm killed 10 „ 

Magnesia killed 7 „ 

Urea killed . . .... 68 „ 

Other organic matter . • . * . 134 „ 


The astonishment with which we regard this attempt is increased 
when we find that the quantities from which these values are 
calculated are not the results of special chemical analysis, but are 
merely averages taken from the standard physiological text-books. 
And it may here be said that the minuteness of Bouchard's 
mathematical calculations can only be valued properly, when it is 
remembered that neither in his lectures nor in his original papers 
is any chemical analysis — upon the accuracy of which they must 
all depend — put forward in their support. 

This theory of division of labour rests upon the idea that the 
effect of small doses is similar to, but weaker than, that of large. 
That this is not so is known to every physiologist. " The effect 
of drugs varies very much according to the quantity employed. 
Sometimes this is due to the interaction of different parts of the 
body on one another, as already mentioned in regard to veratrine. 

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Sometimes it is due to the different effects upon individual cells or 
tissues. Thus we find, very generally, that any substance or form 
of energy, whether it be acid or alkali, heat or electricity, which in 
moderate quantity increases the activity of cells, destroys it when 
excessive. But varying doses do not always produce opposite 
effects. We sometimes find that exceedingly small and exceedingly 
large doses have a similar effect, which differs from that produced 
by moderate doses. Thus, very minute quantities of atropia render 
the pulse somewhat slow; larger quantities make it exceedingly 
rapid, and very large quantities again render it slow. Moderate 
doses of digitalis slow the pulse, larger quantities quicken it, and 
still larger quantities render it slow again." ^ 

Apart from this fallacy, which is quite fatal of itself, Bouchard's 
reckoning is much as if, finding that a man had taken a fatal dose 
of strychnia in an ounce of whisky diluted with water, we should, 
remembering that men have died from swallowing a bottle of 
spirits at a draught, certify that the patient had been poisoned, :5|^ 
by alcohol, f^ by strychnia. 

Considering for the present purpose the one fact of death alone, 
I made a series of analyses of unne to see if any factors could be 
found to vary constantly with the toxic value. In this way I 
calculated the urea, the uric acid, the mineral acids, in a few cases 
the lime salts, and the potash. Thinking that if any organic body 
participated appreciably in the fatal result, it wouJd probably be 
traceable in that small amount of nitrogen which is not due to the 
urea or the urates, I calculated also the total, and thus the residual 

I soon satisfied myself that no other factor than potassium 
varied in harmony with the toxicity. But I was long unable to 
obtain a proportion of this body which should be even approxi- 
mately constant. I at last became convinced that in the best 
method recommended by the text-books ^ there is liable to be a 
loss of potassium, when in the last stage of the process ammonium 
chloride is being driven off by heat from the dried residue of mixed 
chlorides, or else too large a result if the ammonium be not fully 
driven off. I altered the process ^ by distilling off the ammonium as 

1 Lauder Bninton, ' Pharmacology,' 2nd edit., p. 26. 
» Neubauer and Vogel (Hnppert), lOth edit. 

* My process is described in the ' Joarn. Physiol.,' Cambridge and London, 

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ammonia, and have since then obtained results which appear to 
me conclnsiye. I have no doubt that potassium varies constantlj 
with toxicity, and that nothing else does. The results of the last 
twenty analyses are given in the accompanying table. 

The estimation of urea was made by the hypobromite process, corrected for 
atmospheric pressure and temperature, reckonin^^ 1 c.c. of nitrogen » '001868 
grammes of nitrogen and '002952 of urea by weight. 

The urie acid was estimated by (Rowland Hopkin's method. The total 
nitrogen was estimated by Ejeldahl's method, using -^ sulphuric add 
and ^ caustic soda solutions. Chlorine was reckoned by Volhard's method, 
titrating with ^ solution of silver nitrate, of which 1 c.c. = *001 grm. CI ; 
phosphoric acid, by titrating with a solution of uranium acetate, containing 
85*5 grros. to the litre ; sulphuric acid, by adding gradually barium chloride 
solution, containing 80*5 grms. to the litre to 100 c.c. of urine boiled with a 
little HCl, and, after each addition, testing the clear filtrate with mag. sulph. 

The simple sulphates were tested in the same way, except that the urine was 
not heated. The conjugate sulphates were reckoned as the difierence between 
the two results. Lime was estimated by adding ammonia, filtering the pre* 
cipitate after standing, redissolving with acetic acid and adding excess of 
ammonium oxalate. After twelve hours standing the precipitate was burnt 
with the filter to a constant weight. 

To the view held by Feltz and Eitter, and by Astachewsky, that 
death is due to poisoning by potash salts, Bouchard raises several 

First, he asserts that there is not enough potash in the urine to 
produce death in the doses required, and gives the fatal doses of 
the various salts as follows : 

Chloride of potassium, 0*180 grm. per. kilo.. 
Sulphate „ O'lSl „ „ 

Phosphate „ 0'268 „ „ 

As he nowhere gives any chemical analyses of the urines he has 
used, he appears to have arrived at their contents by guess-work. 
In my own estimations the amount of potassium (reckoned as 
E2O) in the fatal dose per kilo, lies in all but four instances 
between 01400 and 02100 grm. The lower amount would corre- 
spond to 0*224 grm. of the chloride, 0*262 grm. of the sulphate or 
neutral phosphate, and 0406 of the acid phosphate.^ Two of the 
remaining four contain larger, and two smaller amounts. The 
lowest (No. 17) might have contained 0188 grms. of potassium 

1 1 grm. KjO will form 1'6 grms. Ka, IB grms. K2SO4, 1-8 grms. KSHPO4, 
2'9 grms. KH3PO4. 

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chloride alone, or 0*211 grm. of the sulphate, or 0"341 grm. of 
the acid phosphate. The mixture, whose proportions, it will be 
remembered, are unknown, would certainly fall little, if at all, 
short of the required total. The next lowest (No. 18) which con- 
tained no sulphates or phosphates had therefore '191 grm. of the 
chloride, which is more than required. The lowest of Beck's fifteen 
estimations contains over -1400 grm. of KjO. Direct estimation 
therefore disposes of Bouchard's first objection. Another series of 
estimations will be found on p. 315. 

It is plain from the table that the proportion of potash is not 
constant, and the same is confessed by Bock. The highest amount 
of potash that he found in the fatal dose per kilo, was *3521 grm., 
the lowest -1432 grm. And it is here proper to inquire whether 
this wide yariation obliges us to suppose varying conditions in the 
urine, or variable reaction in the rabbit. Of this latter factor there 
is no hint in the writings of Bouchard, nor in those of the many 
French observers who have followed in his steps. The following 
tables will show the state of the case. 

Table II. — Injection of saline solution of similar rate and under 
simila/r eonditiom. 

Weight of rabbit. 

Total injected. 

Total retained.i 

Fatal dote per Idlo. 

2900 grms. 



310 C.C. 

2850 „ 

1550 „ 

1200 „ 

491 „ 

2800 „ 

1850 „ 

1610 „ 

676 „ 

2720 „ 

1030 „ 

1030 „ 

878 „ 

2650 „ 

880 „ 

860 „ 

820 „ 

2530 „ 

1560 „ 

1090 „ 

430 „ 

2520 „ 

820 „ 

730 „ 

210 „ 

2450 „ 

1290 „ 

1150 „ 

469 „ 

2100 „ 

860 „ 

850 „ 

404 „ 

In the following coses the rabbits suryiyed 

2850 grms. . . .; 1400 c.c. 

1850 C.C. 

>477 C.C. 

2520 „ ... 2600 „ 

1180 „ 

>468 „ 

2300 „ ... 2260 „ 

1750 „ 

>760 „ 

^ The rabbit is weighed before and after the injection; the increase in weight 
is taken as the amount retained, the rest escapes by the urine, which is paraed 
profusely. 1 grm. is reckoned at 1 c.c. 

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Table III. — Gaaea in which the same urine was injected into two 
rabbits. The injections were made in immsdiate sequence and 
under the same conditions. 

Weight of itbbit. 

Total iiOectod. 



'2150 gmu. . 
■.1850 „ . 

X93 „ 

104 „ / 

6 per cent 

2400 .. , 
.2800 „ . 

166 .. 

68 „1 

6 .. 

170 „ 

73 „ ; 

,2300 „ . 
2200 „ . 

93 .. 

40 „ 1 

11 .. 

100 „ 

45 „ J- 

2660 „ . 

212 „ 

79 „ 1 

12 .. 

.2440 „ . 

220 „ 

80 „/ 

.2400 „ . 

165 „ 

68 „ 1 

12 ,. 

.2800 „ . 

180 „ 

78 „ / 

2630 „ 
■.2400 „ . 

168 „ 

61 ,. \ 

14 .. 

172 „ 

71 „ ; 

'2090 „ 
"2155 „ . 

168 „ 

77 „ 1 

16 „ 

200 „ 

92 .. J- 

1980 „ 
■.2150 „ . 

108 „ 

64 .,1 

16 „ 

140 „ 

66 „ / 

•2410 „ . 
2430 „ , 

176 „ 

72 „1 

17 „ 

212 „ 

87 „ / 

2850 „ . 
12630 ., . 

122 „ 

61 „1 

19 „ 

168 „ 

63 „ / 

faiBO „ . 
\2660 „ . 

144 „ 

46 .. 1 

28 .. 

156 .. 

69 „ / 

/2800 „ 
1.2650 „ 

115 „ 

41 ..-I 

24 „ 

146 .. 

64 „ 

/2870 „ 
12720 „ 

74 .. 

26 ... 

80 „ 

100 ,. 

86 „ 

/2200 „ 
.2220 „ 

143 .. 

66 „ ■ . 

85 „ 

222 „ 

100 „ , 

1-8020 „ 
8580 .. 

183 .. 

44 „ 

88 „ 

256 „ 

71 „ 

f2785 „ 

88 „ 

29 „ • 

89 „ 

18056 „ 

160 „ 

48 „.• 

J 2130 „ 

80 „ 

37 ... 

48 „ 

18450 „ 

226 „ 

65 „ , ■ 

f2840 „ 
12490 .. 

78 „ 

83 „ 

62 .. 

173 „ 

69 „ .■ 

These are not selected cases ; they are all the cases in which I 
have injected two rabbits with the same urine. Two conclusions 
may be drawn : 

(a) That bj a large number of experiments a standard may b € 

^ I have taken as the standard the larger fatal dose in each pair, 
taken the smaller, the variation would have appeared greater still. 

Had I 

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obtained with an approach to accuracy, for in these eighteen cases 
twelve vary less than 25 per cent, from one another. 

(li) That nothing more than this must be expected, and that 
wide variations will occasionally be met. 

A third follows from the fact mentioned on a previous page : 

(c) That these variations will tend to be wider the weaker the 
urine in potash. 

Bouchard, secondly, asserted that the urine killed by stoppage 
of the respiration, and not, like potash Baits, by heart failure. 
That this is not the case has been shown by Beck. . 

Thirdly, Bouchard objects that if potash were alone responsible 
the solution of the mineral ash^ should not be less toxic, as it 
sometimes is, but should have the full toxic value of the parent 
Tirine. But he apparently does not remember that in the process 
of incineration the chloride, which is the most toxic of the potash 
salts, would partly volatilise, and he does not' seem to have ana- 
lysed the ash solution to see if the potash content is the same or 
not. The following are such analyses, which show a loss of potash 
proportionate to the loss of toxicity : 

, r Urine 

' I Ash solution 
2 r Urine 8 . 

* I Ash solotion 
gf Urine < . 

' L Ash solution 

Table IV. 

Kfi '3641 per cent. Fatal dose per kilo., 41 and 54 cc' 

„ -2970 „ „ „ 67 

„ '2679 „ „ „ 66 

„ -2145 „ „ „• 66 and 87 

„ -2506 „ „ „ 88 

„ -2248 „ „ . „ 124 

There is, indeed, a remarkable difficulty about the effect of this 
solution of the ash, but it is very different from that raised by 
Bouchard. It was noticed by Feltz and Eitter, by Bouchard 
himself, and by Beck, that the ash solution is sometimes not less 

1 The dry residue of evaporated urine is fused on platinum, and the crystal- 
line product treated with hot water. It will not all dissolve. Filter and make 
up the filtrate to the original volume hy repeatedly washing the precipitate on 
the filter. The filtrate is clear and alkaline, contains chlorides, phosphates, and 
sulphates, with alkalies, hut gives no precipitate with ammon. oxalate. The 
precipitate on the filter dissolved in acetic acid gives a copious precipitate with 
excess of ammon. oxalate. 

s Where two values are given two rabbits were tested, 

* No. 11 in Table I. 

* No. 20 in Table I. 

Digitized by 



bat more toxic than the original urine. The following instances 
have occurred in the course of mj injections : 

Table IV — continued. 

4/ Urine . 
* I Ash solution 

. K2O — 



Fatal dose 



., 54 and 65 c.c 

»» —" 





K f Urine 
' I Ash solution 

. „ -1684 




. „ 1418 




gf Urine . 
I Ash solution 




77 and 91 ,. 




41 and 46 „ 

7/ Urine 
' l Ash solution 





*» "" 





In these last four cases there has been present, during the injec- 
tion of the ash solution, a symptom that I have never seen except 
in them, — slow, irregular spasms of various parts, one after the 
other, resembling the '* athetoid " movements seen in old cases of 

On the other band, in the three cases before given, and in the 
following : — 

Q r Urine ' • • KjO '3420 per cent. Fatal dose per kilo., 43 c.c. 
I Ash solution . „ — „ „ „ 52 „ 

the toxicity has been what might have been expected, a little less 
than that of the parent urine, and there have been none of these 
curious " athetoid " spasms. To what they and the great increase 
of toxicity are due I do not know. Bouchard suggests that the 
carbonates are increased ; but when I tested the ash solution by 
acidulating, boiling, and passing the vapour through baryta water, 
the reagent was only rendered faintly opalescent. They could only 
increase at the expense of the chlorides, and the toxicity of the two 
is described as equal by Ringer.^ Beck thinks that the absence of 
urea prevents urination, and that, the whole of the potash being 
now retained, the solution kills more quickly than the urine. But, 
at the rate at which I inject, my rabbits never pass more than a 
few c.c, often none ; and moi-eover, they sometimes urinate during 
the injection of the ash solution. A second suggestion of 
Bouchard is that the organic constituents burnt off in calcination 
counteract the potash salts. In any case the effect is not constant. 

» No. 13 in Table I. 

a 'Handbook of Therapeutics,' 12th edition, p. 177. 


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Others do Dot mention these peculiar convulsions that I have seen, 
so that thej may have been accidental, but it is odd that thej 
should have occurred in those very cases wherein the poison was 
greatly stronger. There is a certain curious antagonism between 
lime and potash salts, and I thought once that the absence of lime 
might heighten the effect of the potash, but the idea was not 
borne out, either by direct experiment or by the other cases in 
which the ash solution produced no such symptoms, though it was 
destitute of lime. 

Bouchard's fourth objection is that urine filtered through animal 
charcoal loses one third of its toxicity, but only one sixteenth of its 
potash. In the absence of all detail, and in the absence of any 
chemical analysis, I have not thought it worth while to repeat this 
experiment. Every chemist knows that this carbon behaves very 
variably when used in different ways, and that it is impossible 
without direct analysis to say what is in the filtrate, or, what, or 
how much, is retained. 

Fifthly, he objects that if evaporated slowly, urine becomes not 
proportionately, but absolutely more toxic, which he ascribes to 
changes in organic compounds. But this is a known law for potash 

" The poisonous action of potassium, sodium, ammonium, and 
some other salts depends mainly on the percentage dose, not on 
.the total amount conveyed to the heart. In experiments on the 
frog's heart, when sufficient of the fluid is added to the circulating 
blood to cause arrest of contractility, this annulled property can 
be restored by diluting the blood with an equal quantity of saline 
solution, so that the ventricle receives the same quantity of the 
salt, but in a more diluted form."^ 

It has been maintained by Mairet and Bosc ^ that a large part 
of the fatal effect was due to the pigments, which they obtained by 
precipitating with lead subacetate. This precipitate, extracted and 
purified, they re-dissolved in water and injected. But the precipi- 
tate so prepared is not pure,^ and its effects cannot be considered 
as those of the pigment. Lapicque and Maretti* found no con- 

^ Ringer, ' Handbook of Therapeutics,' 12tlj edition, p. 129. 
^ 'Arch, de physiol. norm, et path.,' Paris, tome iii, p. 273. 

* A. E. Qarrod, ** A Contribution to the Study of the Yellow Colouring Matter 
of the Urine," * Proc. Roy. Soc. London,' vol. Iv, p. 394. 

* * Compt. rend. Soc. de Biol./ Paris, 1894, s^r. 10, tome i, p. 598. 

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nection between the degree of colour tested by the colorimeter and 
the degree of toxicity. 

Dr. Archibald Garrod was so good as to give me a specimen of 
the yellow pigment of the urine (urochrome is the name given it 
by its first discoverer, Thudiehum) dissolved in alcohol. He could 
not tell me the exact quantity of urine employed to obtain it, but 
it was many hundred cubic centimetres. 

To dissolve this in distilled water (after evaporation of the 
alcohol) would have produced a fluid so unlike the normal urine 
that injection would have given no certain results. I preferred, 
therefore, to dissolve it in urine. The result was as follows : 

1. Rabbit. — Weight 1870 gnns.; temperature 102'4® F. Urine at tempera- 
tnre of room was injected into the auricular vein. 

At 10 c.c. — The pupils hegan to contract. 
At 30 c.c. — Twitching of neck muscles ; respiration slower. 
At 60 c.c. — Respiration stiU slower and a little embarrassed; slight stool and 
a very little urine. 

At 85 c.c. — Convulsions ; exophthalmos. 
At 86 c.c— Pupil a little dilated ; death. 
Duration of experiment eleven minutes ; temperature at death 102*6° F. 

2. Rabbit. — Weight 1870 grms. ; temperature 102*8° F. Same urine. 
At 20 c.c. — The pupils hegan to contract. 

At 30 c.c. — Twitching of neck muscles. 

At 40 c.c. — Respiration slower. 

At 80 c.c. — Respiration irregular; a slight stool and a little urine. 

At 122 c.c. — Convulsions ; exophthalmos. 

At 125 c.c. — Convulsions; pupils widely dilated; death. 

Duration of experiment sixteen minutes; temperature at death 102*6 F. 

3. The yellow pigment described above, dissolved in alcohol, was evaporated 
below boiling-point on a water-batb, and was re-dissolved in 200 c.c. of the 
same urine. 

Rabbit.— Weight 1550 grms. ; temperature 101*6 F. 

At 25 c.c. — The pupils began to contract. 

At 55 c.c. — Twitching of neck muscles. 

At 90 c.c. — Respiration very low. 

At 95 c.c.-^Convulsions began. 

At 100 c.c. — Exophthalmos; pupils dilated; death. 

Duration of experiment fourteen minutes; temperature at death 101° F. 

The post-mortem was made carefully in each case, and the organs were 
natural. The heart was dilated in the last case, the body being opened imme- 
diately ; but in the first two, which were made nearly an hour after death, it was 
contracted. This 1 have always found to occur after this interval. 

The toxic values were— (1) 46*98 c.c. per kilo. ; (2) 66*84 c.c. per kilo. ; (3) 

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4'51 c.c. per kilo. Thas the addition of more than doable the previons amount 
of yellow pigment did not increase the toxicity. The absence of any loss of 
temperature in the first two is a very uncommon thing. The experiment was 
done in Jane, 1896. 

A similar experiment was performed with nroerythrin. I need not give full 
details. The injection was made on 9th July, 1896, a very hot day. 

1. Babbit.— Weight 1680 grms. ; temperature 103'2° F. Normal urine killed, 
with convulsions, at 83 c.c. ; duration of experiment twelve minutes ; tempera- 
ture at death 103*4*' F. 

2. Rabbit.— Weight 2050 grms.; temperature 103*6° F. The same urine 
killed, with convulsions, at 112 c.c; duration of experiment thirteen minutes; 
temperature at death 103*6° F. 

3. To 200 c.c. of the same urine '0080 grm. of nroerythrin was added. This 
had been given me by Dr. Garrod. It was extracted by him ^ in alcohol, kept in 
a coloured stoppered bottle in a dark place, evaporated in a dark room at 88° C, 
and re-dissolved in the urine. 

Rabbit.— Weight 2120 grms. ; temperature 102*4° F. 127 c.c. were injected. 
The respiration was now slow and irregular. As the purpose of the experiment 
was fulfilled, the injection was stopped, and the rabbit recovered. 

The toxic values were as follows : — (1) 49*40 c.c. per kilo. ; (2) 64*63 c.c. per 
kilo. ; (3) more than 59*90 c.o. per kilo. 

A similar experiment was performed with urobilin in June, 1896. 

1. Rabbit. — Weight 2400 grms.; temperature 104® F. Normal urine killed, 
with convulsions, at 165 c.c; duration of experiment fifteen minutes; tempe- 
rature at death 103*2° F. 

2. Babbit.— Weight 2800 grms.; temperature 102*8° F. The same urine 
killed, with convulsions, at 170 c.c; duration of experiment twenty- four 
minutes; temperature at death 102*2° F. 

3. To 200 c.c. of this urine was added the urobilin extracted by Dr. Garrod ^ 
from a much larger quantity of urine. It had been preserved in chloroform 
and alcohol, was evaporated on a water bath, and was dissolved in the urine by 

Rabbit.— Weight 2200 grms.; temperature 102*8° F. This urine was fatal, 
with convulsions, at 172 c.c; duration of experiment twenty-three minutes; 
temperature at death 102° F. 

Toxic values:- (1) 68*75 c.c. per kilo.; (2) 73*91 c.c. per kilo. ; (3) 78*63 co. 
per kilo. The post-mortem examination was made in every case with a nega- 
tive result. 

These experiments, made with the purest pigments hitherto 
extracted from urine, prove that their addition in quantity, which 

1 For his method see * Journ. Physiol.,* Camb. and Lond., vol. xvii, p. 439. 
^ For his method see ibid., vol. xx, p. 112. 

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is proportionately very large, does not increase the toxic value of 
normal urine.^ 

But the actual cause of death was not the only point on which 
Bouchai'd held novel views. 

He asserted that the urine of sleep differs from that of waking 
hours, both in the quantity and the quality of its poisonous property ; 
that the urine of sleep is less toxic, and is also more convulsant 
than that of day ; and that if the two be mixed the toxic value of 
the mixture will not be equal to, but less than, that of the propor- 
tionate mean between the two. He founded upon this an ingenious 
theory that sleep was the result of a chemical poisoning. During 
the day he supposed mankind to form a narcotic substance within 
their system which, gradually accumulating in the blood, made 
them sleepy ; while during sleep, " a convulsive substance is 
elaborated, which, when accumulated, could produce muscular 
twitch ings and induce waking." * As usual, he produced no 
chemical grounds for this view. 

The following cases show — 

(a) That the urine of night is less toxic than that of day in pro- 
potion as it contains less potash. 

(h) That there is no such qualitative difference as Bouchard 
claims, but that both somnolence and convulsions occur in equal 
proportion with each urine. 

1. Urine, 8 a.m. to midnight, 1190 o.c; clear, amber, acid; sp. gr. 1015; 
urea 1*3 per cent. ; uric acid '0391 per cent. Rabbit 2860 grms. Fatal dose 
280 c.c.»98 c.c. per kilo. Somnolent till just at the end, when it had the usual 
convulsious and died. 

Urine, midnight to 8 a.m., 450 c.c. ; slightly hazy, amber^ acid ; sp. gr. 1022 ; 
urea 2*1 per cent. ; uric acid '0734 per cent. Babbit 2700 grms. Fatal dose 
290 c.c. =107 c.c. per kilo. Somnolent till just at the end, when it became con- 
vulsed and died. 

2. Urine, 8 a.m. to midnight, 795 c.c; clear, amber, acid; sp. gr. 1020; urea 
2*1 per cent. ; uric acid '056 per cent. Rabbit 3010 grms. Fatal dose 150 c.c. 
^«49 c.c. per kilo. Somnolent until 120 c.c. At 140 c.c. convulsions began, 
which ended in death. 

Urine, midnight to 8 a.m., 615 c.c; turbid, pale, amber, neutral; sp. gr. 

^ The toxic values given above must not be taken as the toxic value of the 
excretion of twenty-four hours. Tl e urine was that passed during a part only 
of the day. 

' Oliver's translation, p. 41. 

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1016 ; urea 1*7 per cent. ; uric acid -060 per cent. Rabbit 1960 grms. Fatal 
dose 300 c.c.»15d c.c. per kilo. Slight drowsiness only, and for a short time. 
At 300 c.c. there were slight convolsions, ending in death. 

3. Urine, 8 a.m. to midnighti Oct. 28, 1897, 870 cc; clear, amber, acid; 
sp. gr. 1020; urea 1'9 per cent.; uric acid '070 per cent.; KjO '3182 per cent.^ 
Rabbit 2360 g^ms. Fatal dose 180 c.c. ==76 cc. per kilo. No somnolence. 
Convulsions began at 170 cc, and ended in death. 

Urine, midnight to 8 a.m., Oct. 28, 1897, and the same hours, Oct. 29, 1090 c.c; 
slightly turbid, pale, amber, slightly acid; sp. gr, 1013; urea 1*7 per cent.; 
uric acid *043 per cent. ; E3O '1098 per cent. Rabbit 2710 grms. Fatal dose 
400 cc 3=147 cc. per kilo. Drowsy from 60 c.c. to 300 cc Death with con- 
vulsions. Rabbit 1900 grms. Fatal dose 870 cc.= 184 c.c per kilo. Drowsy 
from 70 c.c. to 270 cc. Convulsions began at 300 c.c, and occurred at intervals 
until death. 

4. The analyses are given in Nos. 14 and 15 of the table. Urine of 8 a.m. to 
midnight, Jan. 17 — ^No. 14. The Rabbit, 3070 grms., was drowsy from 40 cc 
to 100 cc Convulsions occurred at 170 cc, and wore repeated at 190 .cc, when 
they proved fatal. Urine of midnight to 8 a.m., Jan. 17 and 18— No. 15. The 
Rabbit, 2720 grms., was drowsy from 30 cc. to 70 c.c, and again from 190 c.c. 
to 300 cc No convulsions occurred before 420 c.c, when the experiment was 

5. The analyses are Nos. 16 and 17 in the table. Urine of 8 a. m., to midnight, 
Feb. 5— No. 16. Rabbit 1098 grms. No somnolence. Convulsions began at 
80 cc, and were fatal at 98 cc. Urine of midnight to 8 a.m., Feb. 5 and 6 
— No. 17. Rabbit 1760 grms. Drowsy throughout the injection ,until at 
150 c.c. convulsions began, which ended in death at 169 cc 


Beck performed many more experiments on this point than I, 
and entirely confirms the second of my conclusions. He does not 
appear to have made comparative chemical analyses of the two 
urines. But he did what I find I have omitted, namely, mixed 
the urines, and found that the toxicity of the mixture was actually 
the proportional meau of the toxicity of its components. In this 
point also, therefore, he was unable to confirm Professor Bouchard's 

Bouchard further attempted to establish the existence of many 
poisons in the urine, each with its appropriate and peculiar symptom. 
Firstly, there is a diuretic substance ; secondly, a narcotic ; thirdly, 
a sialogenous ; fourthly and fifthly, two convulsant substances ; 
sixthly, something that produces miosis ; and, lastly, a body that 
reduces temperature. The simplest way to consider them is to 
consider the various symptoms which occur during the injection. 

' Analysis by old method. 

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1. Miosis nearly always occurs with urine. It begins quite early 
and becomes extreme. In four different urines, extracted by alcohol 
after evaporation, I have never seen it occur either with the alcoholic 
or with the watery extract. It does not occur with the solution of 
the ash. It is said not to occur with urine that has been boiled.^ 
I have several times distilled urine, and find that the distillate 
does not produce it. Once I made up the residue, which had been 
boiling a long time, to its original volume with water, and after 
filtration injected it. This urine contracted the pupil ; but it is 
the only note that I have on this point with boiled urine. Miosis 
may occur at the end of large injections of saline solution, but this 
is probably from some cause quite other than in the case of urine. 
It occurs with all urines, whether of herbivora or carnivora.* 

2. Urination has usually, not always, occurred during the injection. 
The amount has been insignificant, perhaps because my experiments 
have rarely taken so long as twenty minutes. The urine so passed 
does not contain the poison,' and hardly any urea. Out of eight 
injections of ash solution, urine has been passed in four. It has 
occurred both with the alcoholic extract which contains all the urea, 
and with the watery which contains none. It occurs profusely with 
large injections of saline solution, and it occurred with injections 
of sulphate and chloride of potash dissolved in saline solution. It 
has, therefore, no special significance. 

3. The passage of fseces, in which the motion has sometimes 
been very loose, has often occurred during injection of urine, and 
also in injections of the alcoholic extract ; but I have not seen it 
either with the watery extract or with the solution of the ash. It 
is quite possible that urea may play a small part in producing these 
two symptoms. 

4. I have only noted salivation in injections of the alcoholic 
extract, and in one urine, No. 3 in the table. 

5. Drowsiness occurs very commonly with urine ; it occurs with 
injections of the ash solution, and it occurs with injections of 
potash salts dissolved in saline solution. 

6. Convulsions occur with urine, with alcoholic and watery 
extracts, with the ash solution, and with salts of potash dissolved 

^ Lapicque and Maretti, 'Compt. rend. Soc. de Biol.,' Paris, 1891, s^r. 10, 
tome i, p. 598. 
^ Gainard, 'Compt. rend. Soc. de Biol./ Paris, 1898, s^r. 9, tome v. 
» Guinard, ibid., p. 489. 

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in saline solution. They often begin Tvith backward jerks of the 
head. A measure of their prevalence in anj experiment may be 
made by noting the point at which the fii*st of these spasmodic 
jerks takes place, and the point at which death occurs. Beckoning 
in this way the last twenty cases, which are those giren in the 
table, I can find no strict rule. 

Table V. 

No. 15 had no convulsions ; 420 c.c. were injected. The rabbit survived. 
„ 19 had one convulsion at death. Total given, 100 c.c. 


2 had convulsions for the last 5 c.c. 

















203 „ 
105 „ 

83 „ 
159 „ 
180 „ 

98 „ 
228 „ 
190 „ 
155 „ 
240 „ 
145 „ 
245 „ 
234 „ 
800 „ 
190 ,. 
120 „ 
260 „ 

It is obvious that, though there is a slight tendency for the weaker 
urines to allow longer time for convulsions before they produce 
death, yet this has many exceptions. 

Death always, in my experience, occurs with some convulsive 

7. The loss of temperature is almost always found, but not 

With injections of 1400 to 1800 c.c. of saline solution, warmed 
nearly to blood heat, the loss is only about 1'3° C, though the 
injections took more than an hour. With injections of urine 
warmed to the same heat the loss varies from nothing up to 1^ C. 
With injections of urine, at a temperature of the room, the loss 
varies from 0*4*^ C. to 2*7° C, but of twenty-one cases only two 
lost as much as 2° C. 

Guttmann thought that potash salts lowered temperature, but 

Digitized byCjOOQlC 


this seems uncertain. At anj rate, the injection of a mass of cold 
fluid, together with the weakening of the circulation and em- 
barrassment of breathing, are quite enough to account for the loss. 
Bouchard elaborately calculates that the calorics subtracted bj the 
injection are insuflicient, but appears to take no account of the fact 
that the heat-producing organs are crippled. 

On a review of the whole, I see no valid ground for concluding 
that any urinary constituent but potash is actively concerned to 
produce any of these symptoms, with the single exception of miosis. 
This is as yet unexplained. 

I have already alluded to Bouchard's statement, that a healthy 
man of 60 kilos, excreted in the twonty-f our hours sufficient urinary 
poison to kill 24 kilos, of rabbits. With a pretence of mathematical 
accuracy which frequently disfigures his lectures, he calculates 
that, if that be the case, each kilo, of the man will excrete enough 
to kill 0*4 kilos, of the rabbit. The dose that is fatal to a kilo, he 
has named a " urotoxy," and the amount of poison excreted by each 
kilo, per diem he calls the " urotoxic coefficient." The standard thus 
set up has obtained a considerable vogue in France, and I have 
seen it quoted in American publications, but I am not aware that 
it has been treated seriously in Germany or in England. 

It has already been shown that the urinary toxicity is, in the 
healthy subject, merely an inexact expression of the excretion of 
potash. The injection of rabbits can, therefore, never take the 
place of chemical analysis. But it is as well also to examine how 
far the ** urotoxic " excretion bears out the possibility of fixing a 
standard for health. The following table is calculated from the 
results of injection in a healthy man of 11 stones (70 kilos.), who 
enjoyed excellent health throughout, and who led an active 
professional life. The total of urotoxies excreted is calculated 
from the dose of the urine fatal to the kilo, of animal, and, where two 
injections were performed, from the mean of the two results. (See 
Table VI.) 

These three series, exclusive of the days on which citrate of 
potash was taken for experiment, were conducted under conditions 
of uniformity as great as, and in the last case greater than, occur 
in ordinary life. Dining well means four or five courses with a 
pint of champagne or some other wine; frugal diet means very 
little meat once a dav and no wine. 

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Table VI. 



1 ' 






March 15 . 


1 Dined sparingly. 



16 . 


1 Dined welL 

17 . 


Dined well. 



18 . 


'Dined well. 



19 . 


Dined sparingly. 


20 . 


; Dined sparingly. 


21 . 


Dined sparingly, 
in couotry. 

Half a day's exercise 



22 . 


Dined sparingly. 


23 . 


pined sparingly. 


24 . . 


1 Dined sparingly. 


25 . 


Dined well. 


26 . 


Dined well. 


27 . . 


Dined well. 


4 . 


Dined sparingly. 


5 . 


pined sparingly. 


6 . 


pined sparingly. 


7 . 


Dined sparingly. 
' during the day. 

Pot. citrat., 2 drins. 

June 1 . 

i 20-5 

Very frugal. 


2 . 

1 226 

jVery frugal. 


3 . 

; 20-2 

Very frugal. 



4 . 


Very frugal. Pot. 
1 the day. 

citrat., 1 drm. during! 


5 . 


Very frugal. 


6 . 

Dined well. 


7 . 

; 16-8 

Very frugal. 


8 . 

! 171 

Very frugal. 


9 . 

' 15-2 

Very frugal. 


10 . 

1 17-2 or 25-7 > 

Dined well. 


11 . 


pined well. 


During the ^ 

rst series the 

potash was estimated for me.^ The 


s are gi\ 

en below with the fatal dose per kilo. (See 

Table VH.) 

It is plain from these figures that even with the diet of ordinary 
life the excretion maj vary from 27*8 to 15*2 urotoxies per diem, 
a variation too wide to admit of any standard. But in sick persons 
the diet is even more restricted, and therefore the excretion will 
be still lower. Thus in a man set. 38, who lay in the hospital with 
symptoms of pressure on his left bronchus, due to a small aneurysm, 

' Very discrepant results from injections. 

' I do not know the method employed in the analysis. 

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Table VII. 


FaUl dote per kilo. 


K,0 faUl per 

March 15 . 

61*9 c.c. and 716 c.c. 


0-1956 g.> 


16 . 

40*4 c.c. and 45*4 c.c. 




17 . 

97-2 c.c. and 104-3 c.c. 




18 . 

61-9 C.C. 




19 . 

87-5 c.c. 




20 . 

115 c.c. 




22 . 

79*6 c.c. and 90*1 c.c. 




23 . 

51-9 c.c. and 63-8 c.c. 




24 . 

68-7 c.c. and 782 c.c. 




25 . 

116-4 c.c. 




26 . 

50-5 c.c. 




27 . 

53-8 c.c. 



who took the dieta dimidia of the hospital, and was treated with 
small doses of potassium iodide, the excretion was — 

Oct. 22 
„ 25 
„ 27 

Nov. 3 

Another man, set, 

13-3 urotoxies. 



170 „ 

29, who was suffering from neuromimesis, and 
who was living upon the same diet and took no drugs, excreted — 

Dec. 30 

„ 81 

Jan. 1 

14*5 urotoxies. 
9-0 „ 
8-0 „ 

I have little doubt that rest in bed, bj lessening both tissue 
change and appetite, will greatly lower the potash excretion of any 
person, and, since we do not know to what extent this takes place, 
we must conclude that, even though a standard were possible in 
health, which it is not, it could not be usefully applied to disease. 

A last question remains, whether the symptoms produced in 
animals by intra-venous injection of urine can be compared with 
those of uTflBmia. It is obvious that there is no necessary connec- 
tion between the two, for the circumstances are different, and, 
though the symptoms found in the one are certainly found in the 
other, yet this may be but an example of the well-known rule that 
similar effects may have many different causes. I propose to put 
the question to the test of analysis, but the difficulties attending 

* Beckoned from the smallest dose fatal. 

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sucli an inyestigation are so great and so numerous, that the result 
must be very doubtful. I am not unaware, moreover, that such 
analyses have, to a small extent, been already made without lead- 
ing to any positive conclusion. March 21«f, 1899. 


dose per 







cc. 160 






















































f — 











L . 

Chabt I shows the percentage of potash, marked by crosses, and the 
fatal dose per kilo, marked by dots, in the twenty cases given iu 
Table L The order is that in which they were performed. 

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Fatal dom 


p«r kilo. 

per cent 



















































































Chabt II gives the same resalts, but arranged according to the fatal dose.' 

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Fatal dose 
per kilo. 



































































Chabt III is composed from Table III. It contains the resnlts of 
eighteen cases in which two rabbits were killed by the same nrine. 
They are arranged according to the smallest fatal dose. It will be 
seen that the variation is greater than that of Chart II. 

The object of the Charts is to show — first, that there is a very close 
correspondence between the percentage of potash and the toxicity of 
the urine; and secondly, that, though this correspondence is broken 
by occasional aberrations, these are actually less than the variability 
of the rabbits themselves would lead us to expect. 

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Path. Soc. Trans. Vol. L. Pl. X. 


Fig. 1. 

Fig. 3. 

Fig. 2. 

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f 1 ' • 'I- 

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Illustrating Mr. Barwell's paper on a case of Congenital Liinb 
Deficiency and Bedundaucj. (Page 320.) 

Fio. 1. — Skiagram showing osseous deformities of left band. 
Fie. 2. — Photograph showing the deformities of both upper extremities. 
FiO. 3. — Skiagram showing bony deformities of right upper extremity. 
(Stereoscopic skiagrams by Mr. Mackenzie Davidson.) 

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1. A case of congenital limb deficiency and redundancy , 
By K. Babwell. 

[With Plate X.] 

A GOOD many years ago I brought to the notice of this Society 
(* Path. Trans./ 1881, p. 280) " Two cases of truncated arms 
bearing at the ends fcetal hands voluntarily mobile," and took the 
opportunity of pointing out the errors of Montgomery, Simpson, 
and many other writers in ascribing these truncations to intra- 
uterine amputation, the latter even going so far as to call the minute 
finger-ends seen at the termination of such abbreviated limbs " rudi- 
mentary reproductions." It is not desirable now to trouble the 
Society with a recapitulation of this paper further than to say it 
pointed out that by far the larger number of truncations were due 
to a peculiar arrest of development, and it ended thus : " I believe I 
know how this arrest is achieved, but must give the matter a little 
more study." Advantage has since been taken of such opportunities 
as have presented themselves, and a few weeks ago there came under 
my notice a girl who bears in her one body a set of congenital 
deficiencies which go far to confirm the views thus alluded to, and to 
clear up some lacune in our rather deficient knowledge of limb 

In this matter the members will be very much assisted by the 
very excellent work of Mr. Mackenzie Davidson. He has taken a 
number of stereoscopic skiagrams of these limbs, showing in almost 
startling realisation and relief the various osseous defects. He has 
further kindly promised to give to the members, who I hope will 
by-and-by examine these Eontgen shadows, demonstrations of his 
methods. In the meantime, I show by lantern the external appear- 

The girl, pictures of whose upper limbs are now seen, is 16 years 
old, rather small and short, but not mentally deficient. Her right 

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hand and forearm are almost entirely absent ; they are represented 
by an addition to the upper ann of a fleshy cushion, which she can 
flex, extend, and to a slight degree rotate (Plate X, fig. 2). At each 
distal comer of this somewhat quadrilateral cushion is a small conical 
projection bearing lilliputian nail-beds, showing that they represent 
the tips of the original limb-buds as they appeared about the twenty- 
fourth or twenty-fifth day of foetal life, only of somewhat larger size. 
We go on to the osseous defects, but let me first remark that it is very 
difficult to isolate and localise specific points in the flat shadow, 
whether cast by the Rontgen ray or by sunlight, of a cylindrical 
object. Mr. Davidson's method of stereoscopic skiagraphy eliminates 
this difficulty almost entirely, and by this aid members will be able to 
see that the lower end of the humerus, although not greatly deformed, 
is abnormal chiefly in the flattened form of the trochlea, and indeed 
of the whole articular end. The ulna is represented by a somewhat 
triangular piece of bone barely two and a half inches long, beginning 
above in a misshapen olecranon and ending below in a button-like 
enlargement ; the surface nearest to and perhaps articulating with 
the humerus is only very slightly concave. The radius is entirely 

There is, however, in this little apology for a wrist and hand a 
small curved piece of bone, a little over an inch long, so placed 
slantwise in the cushion-like appendix, that one end lies quite near 
the base of the inner undeveloped digit, the proximal end lying 
outside, and a few lines below the button-like end of the ulna, and 
this is all that represents the twenty-nine bones of the limb seg- 
ments (Plate X, fig. 3). 

A few words as to my views on the production of this condition, 
although I must revert to the subject, may here be interpolated. I 
hold that in this, as in all cases not due to the comparatively rare 
intra-uterine amputation, the limb-buds duly appeared about the 
twenty -fourth to the twenty-fifth day of intra-uterine life, and then 
when that edge, which afterwards should become finger-tips, pro- 
jected, formative energy ceased; that is to say, just within the 
Wolffian ridge no more cells or clumps of cells, the foundation and 
forerunner of each future bone, were deposited. The period or 
duration of this stasis in formative energy is measurable by observ- 
ing at what distal point of the limb the deficiency begins and at what 
proximal part it ceases. 

We turn now to the right lower limb. It is at once evident that 

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here also is deficiency ; it occurs, however, not in the distal segments, 
but in the proximal one. All the distal parts of the limb, from the 

Ftg. 22. 

Almost total absence of right femur. 

upper end of the tibia onward, are as nearly normal as want of use 
will allow ; neither in circumference nor in length is there greater 
difference than may thus be accounted for. 

But there is no thigh. That segment is represented by a volumi- 
nous though short fleshy mass, which proximally is continuous 
and mingled with the buttock, and distally — that is, two or three 
inches in front of, rather than below, the pelvis — merges into a 
slightly narrower part which contains the upper end of the tibia. 
This right limb is short, therefore, by nearly the whole length of 
the femur, and the foot is only a little below the level of the left 


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In skiagraphy it is barely if at all possible to get a very detailed 
sliadow of such a large bone as the pelvis, especially when surrounded 
by massive soft parts. Yet Mr. Davidson has well succeeded in 
obtaining two good views, which in the stereoscope show that the 
pelvis is properly formed. The condition of the acetabulum can 
hardly be seen, as the cavity is occupied by a bone IJ inches 
long which represents the head and a part of the neck of the femur. 
Beyond this is a gap, and then we come to another piece of bone — 
a more or less misshapen condyloid end, articulating with a fairly 
normal tibia. If the condition of the upper and lower limbs of this 
right side be contrasted, it is dear that we have to do with two 
periods of stasis in development which succeeded one another with- 
out intermediate interval. In the upper limb this began, as already 
said, immediately after the first appearance of the limb-bud. 
Certain work I did some years ago, but which I never had the 
opportunity of completing or verifying, led me to believe that the 
germ of every bone is deposited in the limb before that particular 
part is extruded from the Wolffian ridge, and that afterwards, 
although these deposits shape themselves and grow, no foundation 
of any bone is laid. Thus, in regard to these upper limb segments, 
developmental stasis continued until very near the period when all 
the foundations for the forearm bones should have been laid ; then 
very gradually, as seen by the imperfections of lower end of 
humerus and upper of ulna, formative functions returned ; these then 
resumed full activity, a good shaft of the upper arm bone growing 
out of the Wolffian ridge pushed the belated hand, wrist, and fore- 
arm before it beyond and away from the area of depositing work. 

During that period of inactivity in the upper limb, development 
of the lower was proceeding normally until in the ann formative 
activity was gradually resumed, and at that time it ceased in the 
lower, as though a defect, probably inflammatory, in the central 
nervous system occupied in the spinal cord a certain tract which 
slowly travelled down so as to influence the development power of 
successive regions in the mesoblastic elements of the Wolffian ridge. 
In those parts of that ridge which should have formed the femur 
the formative energy never returned. Both thoracic and pelvic 
girdles — but now I speak only of the latter— are not developed from 
this ridge, but in the mesoblast of the foetal body, much as the 
protovertebrflB are formed, the upper part of the femur being de- 
veloped in continuity with it. Hence those parts, having nothing 

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to do with the Wolffian ridge, do not suffer from its defective energy 
and are perfect. 

The condition of the left hand also shows.a series of developmental 
faults which also are instructive. The forearm and wrist are perfect ; 
so also is the thumb and index, as likewise the middle finger down 
to the two terminal phalanges, which are thick and clumsy in form, 
and, as they cast a peculiarly dark shadow, are probably exceedingly 
dense. This finger is closely webbed to the next one on the ulnar 
side. This one, the ring finger, is also normal to the end of the 
first phalanx — the second begins with a very broad joint, and in 
about the middle of its length splits into two branches, standing 
apart from one another at an angle of sixty degrees (Plate X, 
fig. 1). At the end each branch articulates with a similarly bifid 
third phalanx, the two forks of which unite at an angle of ninety 
degrees to form a wide ungual end supporting a broad nail. Thus 
each phalanx roughly resembles a letter Y, the one upright, the other 
inverted, jointed together at the ends of the branches so as to enclose 
an almost circular space. There is no fifth metacarpal bone ; the 
little finger articulates by a side extension of their joint surfaces 
with the metacai-pal bone and with the first phalanx of the fourth 
finger. All these peculiarities are so well seen in the stereo-skiagrams 
in the next room that they need not be further described here ; but 
I ought to mention that, in spite of these inept-looking extremities, 
the girl's sewing is, I am told, exceptionally good and neat. 

A few words about the bearing on fcetal events which may be 
deduced from this hand. It appears that the morbid state of the 
central nervous system, alluded to above as responsible for the 
deficiencies of the right hand was not completely confined to one 
side, but spread itself out somewhat into the other side of the 
cord ; not, however, in a degree sufficient to produce complete stasis 
of development, but only partial deficiency and disorder. Another 
point is worthy of notice. I believe it is generally considered that 
the bones, as well as the muscles of limbs, are developed under the 
sway and influence of ganglia in the motor tract of the central 
nervous system. This hand suggests, though of course it does not 
prove, a different conception, as far as the bones are concerned. 
For the deformity corresponds with the distribution, not of the 
motor, but of the sensory part of the ulnar nerve. 

January drd, 1899. 

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2. The histology of the rheumatic nodule. 
Bj F. J. PoYNTON, M.D., and G. F. Still, M.D. 

IN bringing before this society a paper upon the lustology of the 
rheumatic nodule, we are fully conscious that its structure has 
been already described in detail by many excellent observers ; but 
we venture to think that the descriptions which have been given, 
especially in the text-books of medicine, are based upoA appear- 
ances that are found when the nodule has already passed through 
the earliest stages of its formation, and for that reason undue 
stress has been laid upon the fibrous elements which are then so 
evident. The essential character of the nodule is to be judged 
from its earliest appearances, before the morbid effects of the 
rheumatic poison have been modified to any considerable extent 
by the reactive processes that occur within the body; and it is 
from a study of these earlier phenomena Ihat one sees most 
clearly the closeness of the analogy, perhaps the actual identity > 
which exists between the rheumatic process, as seen in endo- 
carditis and pericarditis with that seen in the nodule, a relation 
pointed out long ago by Dr. Barlow and Dr. Warner. 

It is, then, to the earlier phenomena that we desire to call at- 
tention, and the sections shown have been selected as illustrating 
this stage of nodule formation, and of the allied processes in the 
endocardium and pericardium. 

We may perhaps first be allowed to make a few general obser- 
vations upon the difficulties that are met with in preparing sections 
of the rheumatic nodule, and to call attention to certain staining 
processes which are of value in such an investigation. In the first 
place, as already pointed out, it is necessary to take the newer 
formations, and not those of many weeks' standing, and to ensure 
this it will probably be necessary to take the smallest that can be 
obtained. Further, the section must pass through or at least near 
the centre of the nodule, for, as has been repeatedly demonstrated, 
the microscopic appearances at the periphery are very different 
from those at the centre. It is probable that the difficulty in carry- 
ing out these precautions account in some degree for the dis- 
crepancies in the descriptions which have been published. Finally,. 

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certain colour reactions given by the aniline dyes carbol-thionin 
and carbol-gentian violet give considerable assistance in the study 
of the early formation of the nodule. 

Tho value of thionin as a nuclear stain was first pointed out by 
Martin Heidenhaiu in the " Festschrift fur den fiinfzigen Jahren 
Jubillauuie Herrn Dr. KoUiker."^ If this stain be used for 
recent fibrinous exudations, such as ocQur in rheumatic peri- 
carditis, or in pleurisy, it is found that the exudate stains a pale- 
blue colour, in contrast to the violet blue of the nuclei of the 
cellular elements and fibrous tissues. If this exudation be stained 
by Weigert's fibrin method it will be also seen that the carbol- 
gentian violet gives the usual reaction for thi^J; material. 

It occurred to one of us (F. J. P.) to make use of these methods 
in the investigation of the nodule, and they have proved, we believe, 
of value. 

So far as the naked-eye appearance goes, the smallest nodules 
which can be appreciated either by sight or touch during life are 
by no means the smallest which can be seen after death. It was 
noted on several occasions that where only a few nodules could be 
found on the head during life, numerous minute deposits of the 
same yellowish-pink material were visible at the post-mortem. 
Some of these deposits were more or less rounded in outline, others 
ran together into irregular areas, each with its leash of small 
dilated blood-vessels running up to it, the whole being too small 
to be apprecia1;ed during life. The colour of these minute deposits 
is much less like that of fibrous tissue than that seen in the older 
nodules, which are greyish white rather than yellowish pink. On 
attempting to remove one of these smaller nodules there is con- 
siderable difficulty, for they contain a certain amount of fluid, 
exudative in character, and any squeezing or traction diminishes 
their bulk, so that they are often lost altogether. This difficulty is 
the greater because there is no distinct line of demarcation from 
the surrounding fibrous tissue. 

Turning now to the microscopic details, we should like to point 
out the close resemblance that there is between the appearances 
of an early rheumatic nodule and recent rheumatic peri- and endo- 
carditis when stained by a precisely similar method. 

The sections shown were taken by one of us (F. J. P.) from a 

^ We are indebted for this reference to Mr. Plimmer, bacteriologist to St. 
Mary's Hospital. 

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case that died in St. Mary's Hospital. Three weeks elapsed between 
the first visible evidence of the nodule and the death of the patient, 
and thus, though not in its very earliest condition, it still shows 
distinctly the nature of the early changes. 

All the sections were from tissues fixed in corrosive sublimate, 
they were cut in paraffin, and stained with carbol-thionin. 

In the centre of the nodule there is a homogeneous material 
arranged in layers and free from cellular elements. This stains 
pale blue with carbol-thionin, and gives Weigert's fibrin reaction 
with gentian -violet. We look upon this material as fibrin in the 
interstices of which there was originally fluid. It is the presence 
of this homogeneous \paterial which we wish particularly to empha- 
sise : for, as we have pointed out below, it is this, and not the sub- 
sequently developed fibrous tissue, which is, in our opinion, to be 
regarded as the essential element in the nodule. Compare now 

Fig. 23. 

Fibroni tiBSQe. 

Cellular zone. 

Section of j 

Hjriiions exndato. 

Section of rheumatic nodule of three weeks' duration. 
Drawn under 1" obj., oc. 2. 

with this the exudation on the free surface of the inflamed peri- 
cardium, and the vegetations on the valve, and it .will be seen that 
they have much the same appearance and give the same reaction. 
Away from the centre of the 7io(7w7e towards the periphery, many 

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eellnlar elements become visible encroaching upon tbis fibrinous 
centre; and again comparison with the deeper part of the peri- 
cardial exudation and with the yaJye shows a similar appearance. 
Still further towards the periphery of the nodule fibrous tissue is 
apparent, some of it swollen and hyaline, and in places there are dis- 
tended and tortuous vessels. In the deeper part of the pericardium 
also the distended vessels are very apparent, and the hyaline ap- 
pearance of its fibrous matrix is also distinct. In the valve the 
swollen appearance of the fibrous tissue can also be detected. 

Thus we can recognise in these three sections fibrinous exudation, 
cellular infiltration, and fibrous tissue, and we know that in the 
pericardium tbe sequence of changes is as follows : first, vascular 
dilatation ; then exudation, which in rheumatism is usually fibrin- 
ous ; cellular infiltration ; and, finally, fibrosis. We conclude that 
the same sequence of events occurs in the rheumatic nodule. 

In this way, and in this way only, it seems to us that the oc- 
casional rapid appearance and disappearance of a nodule can be 
explained, for if tbe rheumatic process is rapid and evanescent, the 
fibi-inous exudate is as rapidly absorbed, and the nodule, which in 
such a case is probably not fibrous at all, vanishes. If the morbid 
process be more protracted, then tbe restorative cbanges will be 
slower, and there will be some fibrosis in addition to absorption, 
and the nodule will more slowly disappear. It is of such a nodule 
as this that sections can be most easily obtained. Now and again 
the nodule lasts for many months, and tbe section of such an one 
shows imperfect restorative processes, the fibrous tissue is ill- 
formed and only to be found in patches, a condition which can also 
be observed in some of the old nodules upon the cardiac valves. 

We are aware tbat it has been suggested that the structureless 
material is a product of degeneration in the nodule, but this sug- 
gestion can hardly, we think, be correct, in view of tbe fact that 
the appearance is particularly well seen in the smaller and more 
vascular nodules which are presumably the young ones, and there- 
fore the least likely to degenerate. 

A study of nodules in various stages of development has seemed 
to us to show that this central portion, consisting apparently of 
fibrinous exudate, is tbe basis, so to speak, of the nodule, and it is 
from this, therefore, and not from tbe peripheral portion, that its 
essential character must be judged. Moreover, the comparison 
with the pericardial exudation shows, we think, that the essential 

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change which produces the rheumatic nodule is an actual deposit 
of inflammatory exudation, and one might even go further and say 
that the formation of fibrous tissue is not a necessity : it need not, 
and certainly does not always, occur. This conclusion, drawn from 
the microscopic appearances, is confirmed by the clinical fact that 
a nodule may appear in twenty-four to forty-eight hours, and the 
whole time from appearance to disappearance may, it would seem, 
be only three days. 

Finally, we would suggest, if the occurrence of fibrous tissue 
formation is to be regarded as a late phenomenon and in no way 
essential to the formation of nodules, a view which we think is 
confirmed by the appearance we have described, that it is more 
satisfactory to apply the term " rheumatic " or " subcutaneous " to 
these nodules than to call them "fibrous." 

Apnl 4ih, 1899. 

3. The technique of blood fi^ms. 
By W. C. C. Pakes and E. Howard. 

WE are venturing to bring forward what we consider to be two 
or three improvements in the technique of blood films. 

Firstly, there are two places from which blood may be conveniently 
collected : the lobe of the ear and the back of the finger. The ear 
has considerable advantages ; it is easily sterilised, and rendered 
hypersBmic, and is out of sight of children and neurotic patients, 
as well as being much less sensitive than the finger. The ad- 
vantage of the finger is that it is rather more convenient to the 

The best instrument for pricking the ear or finger is undoubtedly 
a lancet. Ordinary sewing needles, surgical needles, and pen nibs 
are not much good. The lancet, however, is not suitable for constant 
sterilising and may frighten the patients. We have therefore had 
constructed for us by Messrs. Down Brothers what is pi*actically 
the point of a lancet mounted on a needle. It is a hare lip pin 
which has been cut off at the broadest part of the lance head and 
ground and sharpened to represent the point of a lancet. This 
we have found cheap, efficient, and, of course, painless. 

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The ordinarily described **2 Coverslip" method of preparing 
films is not satisfactory. It requires a great amount of practice, 
and even iu the hands of good manipulators is not constant. Dr. 
Hanson some time ago suggested that good films could be made 
by collecting the blood on the edge of a piece of tissue paper and 
drawing it along a slide. This certainly is easy to do and gives 
good results. But the slide has many disadvantages. It is difficult 
to keep clean, is unhandy in the stains, and is bulky when many 
specimens are to be collected and transmitted to the laboratory. 

We have applied this method to the coverslip. If two square 
coverslips are laid edge to edge on blotting-paper and held down 
with a slide, the cigarette paper may be drawn over these as over 
the slide. A still better method is to use IJ-inch by |-inch cover- 
slips. On these excellent films can be made. 

The inconvenience of their lightness we have overcome by having 
a special clip made. This clip consists of a small block of wood 
five-eighths of an inch from the free edge of which a strip of cork is 
inserted. On this strip of cork a piece of brass is pressed by a spring 
so that the coverslips can be held between the cork and brass. In 
order to charge the clip, four coverslips are laid on the wood so that 
one edge rests on the cork, the spring being depressed. On releasing 
the spring the coverslips are held in position. A great advantage 
of this clip is that the coverslips need never be touched with the 
fingers, and that the clip can be held in the most convenient position 
when the films are being made. In fact, it is just as convenient as 
the slide. 

We must here emphasise the fact that clean coverslips must be 
used. These as they are usually sold are not clean enough for 
blood film work. An easy and efficient method is to boil them in 
nitric acid or chromic acid, remove the acid with water, dehydmte 
with and then keep in absolute alcohol. They should be prepared 
for use by picking them out of the alcohol singly and burning off 
the alcohol. They must never be touched with the fingers until 
the films are actually fixed, otherwise the moisture from the hand 
may lake the corpuscles. 

The cigarette papers to bo used should be those that are not 
fastened to the case, as the tarlene or zigzag. Strips about half 
and inch wide should be cut across the ribs, and the ungummed 
edge used for collecting the blood. 

In order to prepare the film, the under surface of the edge of the 

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strip is moved laterally over the drop of blood, care being taken 
not to get any blood on the upper surface of the paper. The end 
of the strip bearing the blood is laid upon one end of the coverslip 
and the blood is allowed to spread out between the two. The strip 
is then drawn slowly to the other end of the coverslip. A veiy 
little practice enables the manipulator to gauge the amount of 
blood required, and thin, even films can be obtained nearly every 

The films are allowed to dry in the air (this only takes a few 
seconds), and are then ready for fixing and staining. 

Whilst admitting that the method we propose requires a certain 
amount of apparatus, we maintain that the advantages far out- 
weigh the disadvantages. The only real essentials are long slips 
or slides and cigarette papers. 

We wish here to call attention to a very excellent single stain 
which was suggested to us by Dr. MacConkey. Muir and Eitchie 
recommend carbol-thionin blue, i. e. 1 grm. thionin blue in 100 c.c. 
of 1 in 40 carbolic in water, as a bacterial stain ; we do not think 
it is very useful for this purpose, but are satisfied that it is extremely 
simple and effective for certain blood examinations. It stains the 
red discs a faint grey, and the nuclei of the leucocytes a distinct 
reddish colour. It can be used equally well after any fixing re- 
agent, a feature common to very few blood stains. It stains the 
young parasites of malaria extremely well, but is, of course, use- 
less for staining eosinophile or basophile granules. It picks out 
blood in tissue very well, but it is slightly apt to precipitate. The 
preparations should not be left in the stain more than three minutes* 
when they should be well washed in water, dried and mounted. 

Wo have exhibited two films, one of leucocyth»mia and the 
other of malaria, to show the characteristics of the stain. 

Mr. Howard, who is shortly going to Africa, has had the accom- 
panying microscope and accessories fitted up for him, and the case 
contains everything which is necessary for the examination of 
blood. ' December 20th, 1898. 

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February 2l8t and March 7th, 1899. 

Bj Pbof. Or. Sims Woodhead. 

MB. Pbesident and Gentlemen, — I have little doubt that many 
of those who take part in this discussion will describe such 
conditions of " pseudo- tuberculosis " aa tbej have had the oppor- 
tunity of studying. Although I must necessarily say something 
concerning the forms of pseudo-tuberculosis that have come under 
my notice, I may say at the outset that it will be my endeavour so 
to put the matter before you that we, as a Society, may see it our 
duty to attempt to do away altogether with this term "pseudo- 
tuberculosis," and eventually, after due consideration, submit a 
nomenclature, the basis of which I hope may be suggested this 
evening — a nomenclature which may assist us not only to get rid 
of some bad terminology, but in giving a foundation of a classifi- 
cation at once accurate and comprehensive of what at present 
must be looked upon as the flotsam and jetsam of the Patho- 
logical theatre and laboratory. 

I have long been of the opinion that at some time or other it 
would be necessary to get rid of the term " pseudo-tuberculosis," as 
its use has been responsible for a good deal of misunderstanding, 
and now, in the light of recent investigation, one feels that it would 
perhaps be better to treat this question in the same free and easy 
manner that the chapter on snakes was dismissed by a certain 
mythical Hibernian historian. On going over the literature of the 
question, however, one finds that it is absolutely impossible to 
dismiss it thus curtly '* that there is no * pseudo- tuberculosis,* " but 

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references to it are so numerous, and the number of conditions 
classified within this term are so numerous, that "pseudo-tubercu- 
losis " is no longer of the slightest value as a term in classification, 
for after eliminating a number of specific conditions which at one 
time were included under this heading, we have still numerous 
pathogenic conditions most varied as to appearance and etiology 
described by different writers as " pseudo-tuberculosis." 

I may as well begin by confessing my own faults, and referring 
to a series of cases which came under my observation during our 
investigations carried on for the Royal Commission on Tuberculosis. 
I do this because I spoke of them at the time as being cases of 
" pseudo- tuberculosis." I may give the notes and photographs of 
one of these specimens that might undoubtedly have been mistaken 
for true tuberculosis had not the conditions under which it oc- 
curred and the microscopic examination given such definite 
indications that it was not really a case of true tuberculosis. For 
the sake of convenience I spoke of the process as being ** pseudo- 
tubercular." In a series of experiments carried on for the purpose 
of determining whether the meat from a certain cow contained the 
specific tubercle virus a guinea-pig died on the second day after 
the meat had been eaten; much too early, therefore, to show 
tubercle as the result of the ingestion of the meat that was being 
experimented with. In this case the following conditions were 
found : " venous congestion of the large intestine and csecum ; the 
solitary glands and Peyer's patches were enlarged and oftdematous, 
and there were small hsemoiThages into their substance ; in these 
glands in the small intestine were white opaque points ; in some 
cases these were scattered over the whole glandular patch; the 
mesenteric glands were slightly enlarged ; the liver was mottled 
with small yellow patches, very irregular in distribution ; in the 
lungs were two yellowish-grey points ; the spleen was normal, but 
the mediastinal glands were evidently enlarged. 

These photographs (taken from portions of the large and small 
intestine of this animal) show extremely well the appearances 
presented; the degenerated patches were much whiter than any 
tubercle nodules that I had hitherto come across, and the breaking 
down was more complete, so that on microscopic examination one 
could not make out even the outlines of any cells in the degenerated 
area ; no tubercle bacilli could be found in any of the lesions, but 
micrococci, especially in the form of diplococci, sometimes slightly 

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elongated, were numerous. Until our attention was drawn to the 
peculiar whiteness of the nodules, Dr. Cartwright Wood, who was 
working with me, and I agreed, that it was probably a case of 
tuberculosis accidently acquired, but when we came to go into the 
history of this series of animals and found that all the others 
were perfectly free from tubercle, and that it was impossible in a 
single lesion to make out any tubercle bacilli, it was evident that 
we must look upon it as some mycosis other than tuberculosis; 
that, in fact, it was not even an atypical tuberculous lesion. Still, 
without having recourse to microscopic examination I- could not 
then satisfy myself that this was not a case of true tubercu- 

In a couple of guinea-pigs inoculated with raw meat from the 
same cow, small nodules were observed in the spleen : in one case 
all the organs except the spleen were perfectly normal, but here 
were several nodules which to the naked eye looked exceedingly 
like small yellow infarctions. On section and microscopical exami- 
nation these nodules were found to consist of three layers or zones ; 
a central or necrotic area in which the cells were dead, had lost 
their outlines, and had become fused into irregular masses ; near 
the margins of this portion were short bacilli, stained by methylene 
blue, but very readily discoloured, some of them appearing almost 
like diplococci, as the ends were so much more deeply stained than 
the central poi*tions ; i. e. there was distinct polar staining ; no 
tubercle bacilli could be made out. Around this central area was 
a zone of shadowy-looking splenic tissue, whilst around this, again, 
is a distinct capsule consisting of connective tissue and leucocytes 
surrounded in turn by fairly normal splenic tissue. In the second 
case the spleen again presented the same nodular infarcted ap- 
pearance, the other oi^ans being quite normal; the central de- 
generating area, however, is larger and the connective-tissue capsule 
is not nearly so distinctly marked ; otherwise this is exactly like 
the specimen already described. 

In another guinea-pig injected with artificial tubercular milk, 
heated to 70° C. for one hour, at which tubercle bacilli are rendered 
innocuous, at any rate as far as guinea-pigs are concerned, the 
animal died eleven days after injection, when it was found that 
there had been peritonitis and adhesions between the visceral and 
parietal serous membranes. In some of the adenoid patches there 
were opaque areas over the adherent surfaces. These opaque 

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patches on microscopic examination were found to consist of tissue 
in an advanced stage of necrosis, whilst around this dead mass 
numerous tissue cells, leucocytes, and micro-organisms were found. 
These micro-organisms were in the form of short bacilli with 
slightly pointed ends, some of them again almost like diplococci. 
The non -stained central band was more marked and the polar 
staining was also distinctly brought out. Here also we have evi- 
dently the necrosis due to the action of an organism other than the 
tubercle bacillus. 

Another specimen (photograph) : a small yellow nodule about 
the size of a millet-seed was found near the surface of the liver 
of a guinea-pig that had been injected with artificial tuberculous 
milk heated to 70° C. for ten minutes. The animal was killed 101 
days after inoculation. On microscopic examination this small 
nodule was found to be made up of a large mass of organising 
connective tissue in which were a number of small blood-vessels ; 
at the margin of the mass were numerous leucocytes and young 
connective- tissue cells iu which the blood channels were larger and 
more numerous than were those in the older fibrous nodule. Not 
a single tubercle bacillus could be found, and there was no 
evidence of caseation or of extension into the surrounding tissues, 
and, in view of the fact that no other evidence of tubercle could 
be found in any part of the body, we were compelled to come to 
the conclusion that this growth was not tubercular. 

As I was engaged on a special investigation, 1 used the term 
" pseudo-tuberculous " very much as a matter of convenience, and 
in order to distinguish this condition resembling tuberculosis from 
the true tuberculosis with which I had to deal, but I was fully 
conscious of the fact that in using this term I was adding to a 
confusion that was already sufficiently great, especially in com- 
parative pathology. 

Whilst on this subject, I may mention one or two other condi- 
tions which, at first sight, were mistaken for tubercular granulations, 
and I throw on the screen a photograph of a small grey area found 
in the muscle of a cow. This patch, or group of patches, rather, 
simulated grey miliary tubercular granulations in the muscle of 
a cow in which the visceral organs were tuberculous throughout. 
On microscopic examination it was found that, although the muscle 
fibres were swollen and had undergone hyaline or vitreous (P) degene- 
ration, there was a slight increase in the number of leucocytes, and 

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the foimation of a fibrous tissue capsule around the dogeneratiog 
area; but there was no true tubercular structure, and tubercle 
bacilli could never be demonstrated in any part of the muscle at 
any stage of the degenerative process. The nature of this change 
may be more distinctly seen in the high-power photograph, from 
which it will be seen that the degenerating muscle has undergone 
a granular disintegration ; this, however, being preceded by a loss 
of striation of the muscle, which becomes homogeneous and swollen 
^ — hyaline. It is evident, of course, that this has nothing to do with 
a true tubercular process, nor is it even pseudo-tuberculosis in 
the widest sense of the term, except superficially and to the naked 
^ye; though it is quite possible that, as in the hyaline degenera- 
tion found in the muscles of the fowl in fowl cholera, tliis condition 
may be due to the action of some micro-organisms . or their 

A doctor friend — a medical officer of health — some five or six 
years ago, shortly after the Epidemiological Congress, startled me 
greatly by assuring me that he had seen an enormous amount of 
tubercle in the lungs of sheep. I mildly suggested that I thought 
there must be some mistake, but he assured me that he had only 
that day confiscated the lungs of some thirty or forty sheep, in every 
single one of which he found well-marked grey tuberculous nodules. 
I asked him to show me one of these, and also to give me his 
authority for supposing that these were tuberculous. He brought 
up one of the lungs, and I at once recognised it as what is called in 
Scotland " hoos,'* small pearly-grey glistening nodules, the result 
of the presence of the Sirongylus filarise, a very common parasite 
in the lungs of sheep. 

On microscopic examination, as no doubt Professor McFadyean 
will demonstrate, these small nodules are found to consist of small 
nematode worms coiled up and suiTounded by proliferating connec- 
tive-tissue cells which exhibit very little tendency to undergo de- 
generative changes, any change being in the direction of the forma- 
tion of fibrous tissue rather than towards caseation. 

The tubercle-like bodies met with in the lungs, the so-called 
** worm-knots" of the Germans, are really due to the action of the 
strongylidse, which may give lise to an actual epidemic in sheep, 
oxen, rabbits, and pigs; and Leuckart quotes a case in which a 
similar condition is described as being met with in the lung of a 
child who suffered from the presence of an organism which is sup- 

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posed to correspond to the Strongylna paradoxus which occurs in 
the lungs of the pig. These strongjles, which are egg-bearing 
nematodes with a short larval existence, are found in the air- 
passages of the auimals mentioned. The ova are said by some to 
be brought by the blood-vessels and to be deposited in the walls of 
smaller bronchi and air-vesicles, where they develop into the worm 
form, then giving rise to the formation of these " pseudo-tuber- 
cular " growths, by the irritation they set up. It appears to be 
much more probable, however, especially as the .ova may some- 
times be found on the mucous membrane of the air-passages, that 
they make their way in by the air-passages, and then, impacted 
in the smaller bronchi, and perhaps even in the infundibular pas- 
sages, give rise to that tissue-proliferation so characteristic of their 
presence. They act not merely as foreign bodies, but also as irri- 
t-ant foreign bodies, as we cannot imagine these animal pamsites 
living without excreting certain products which are probably irri- 
tant ; this irritant, however, appears to be only sufficiently active to 
stimulate the cells to proliferation and to be incapable of bringing 
about the secondary degenerative changes that are so frequently 
associated with rapid proliferation. Hence it is that we have the 
glistening translucent nodules with little tendency to undergo 
caseous or purulent changes. This, as we have said, is a perfectly 
distinct process, and one which should certainly not be called a 
** pseudo-tuberculosis." 

This verminous " pseudo-tuberculosis '* is recognised as a dis- 
tinct pathological condition by comparative pathologists, and it 
would certainly make for greater clearness and simplicity could the 
term ** pseudo-tuberculosis " be dropped entirely, and some more 
specific name applied. Pathology is already burdened with too 
many of these vague and general terms which can only have the 
effect of keeping back a scientific classification and nomenclature. 
This is an even greater drawback in comparative than in human 
pathology, for in human pathology certain terms, though inapt in 
themselves, have come to be endowed with a certain significance, 
and we have gradually come to accept a series of names which, had 
we to commence afresh, we should be dissatisfied with. Comparative 
pathology, however, a field that has been worked with such marked 
success by the modem school of veterinary surgeons, is in many 
places virgin soil ; consequently clumsy and misleading terms may 
be readily dropped, as they have not yet come to be too closely 

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associated with the conditions they denote, and these more recently 
described diseases and conditions may at once receive appropriate 

In the introduction to his article on ** pseudo-tuberculosis " in 
birds, Professor Muir draws attention to the fact that there are 
at least six conditions which have been described as '* pseudo- 
tuberculosis," but he describes a form of ** pseudo- tuberculosis " in 
birds which is probably tbe same as that described by Malassez 
and Vignal, Nocard, and Pfeiffer. This is a point of special in- 
terest, as Malassez and YignaFs experiments were carried on with 
an organism which was separated from a guinea-pig inoculated 
with a portion of a nodule taken from the arm of a tubercular 
child; whilst a number of the cases of " pseudo- tuberculosis " 
described, by other authors have also been produced, by the inocu- 
lation of sputum from tuberculous patients or from milk from 
animals that were supposed to be suffering from atypical tubercle ; 
in others, again, guinea-pigs appear to have been affected ** spon- 
taneously," that is, they have contracted tbe disease quite apart 
from experimentation. This is a poiut of considerable importance 
in connection with my own observations on the pseudo-tuberculosis 
of the guinea-pig which evidently occurred, in certain cases at any 
rate, spontaneously; as, in the animal that died two days after 
inoculation with heated tuberculous material ; whilst another case, 
in which bacilli identical in appearance with those described by 
Nocard, Muir, and Pfeiffer were found, was injected or fed with 
artificial tuberculous milk, consisting of the pounded tubercular 
organs of guinea-pigs mixed with ordinary milk. This apparently 
gave rise to this condition on the eleventh day, thus corresponding 
very closely with the condition presented in Professor Muir's ex- 
periments, though, of course, here we were dealing, not with pure 
<iulture8, but with crude material. 

Dr. Muir points out that this special form of "pseudo-tubercu- 
losis," when met with in the subcutaneous tissue of guinea-pigs, 
takes the form of a ** subacute inflammatory focus which undergoes 
-caseation, and usually softening ; " this extends, as a rule, to the 
neighbouring lymphatic glands, and a few nodules may be found 
in internal organs, usually the liver and the spleen. This disease 
is not necessarily fatal. The most marked feature about it is that 
the cells, both leucocytes and connective tissue corpuscles, undergo 
a very rapid necrotic breaking down. This corresponds to the 


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description already given, whilst, as already observed, the casea- 
tion and softening both take place at a very early stage after the 
inflammatory reaction and leucocyte infiltration, the result being 
that the centre of a nodule becomes almost purulent rather than 
caseous. He also points out, as noted in my cases, that the pro- 
liferative changes are well marked and are confined almost entirely 
to the periphery of the nodule, and he draws attention to the fact 
that, owing to the absence of giant cells, the lesion somewhat 
resembles the glanders nodule, except that in "pseudo-tubercu- 
losis " the softening takes place more rapidl j and is more extensive. 
He also found that the bacilli, as in bacterial necrosis, are usually 
found near the margin of the caseous centre ; they may, however* 
be entirely absent, especially in chronic cases. This accords per- 
fectly with what I observed in the " pseudo-tuberculosis " of 
guinea-pigs described in the Report to the Eoyal Commission on 
Tuberculosis, and I now greatly regret that, owing to pressure of 
other work connected with the Report, it was impossible to follow 
out the study of the bacteria producing this disease. I shall, 
therefore, say nothing further about this, beyond expressing my 
belief that the disease we met with was identical with the tvhercu- 
lose zoogloeique of Malassez and Vignal, Nocard, Pfeiffer, and 

In comparatively recent years those of us who have had the 
opportunity of examining cases of actinomycosis have, in searching 
for corresponding cases in our museums, come across casea 
labelled " tuberculosis," which, having the more recent cases before 
you, have at once been recognised as being cases of actinomycosis ; 
whilst there have been brought under the notice of pathologists in 
this country, by Prof. Boyce, of Liverpool, a case which he very 
properly describes as aspergillo-pneumonomycosis, a much better 
term than that given to a similar condition by Kotljar, who 
describes what he terms an aspergillo-pseudo-tuberculosis. 
Kotljar, indeed, insists specially that these " pseudo-tuberculoses " 
can be divided into two groups, those of bacterial origin, and those 
of mycotic etiology, these latter being produced by aspergilli, 
especially probably the Aspergillua fumigatus. 

Here, again, we are at once led into difficulties when we come to 
consider these different forms of " pseudo-tuberculosis." During 
life it is impossible to find the tubercle bacillus in the expectora- 
tion, whilst, as is well known, there are a number of cases on 

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record in wbicb an aspergillus has been found in the sputum 
directly it comes from tbe lungs. In birds and animals this 
condition of pneumonomjcosis is of comparatively common occur- 
rence, and tbe term used by Boyce is certainly mucb preferable 
to aspergillo-pseudo-tuberculosis. Even when we come to tbe 
bacillary psetLdo-ivherculosis ovis^ or pseudo-tuberculosis of sbeep, 
the inconvenience of using a term which applies to a pathological 
condition so entirely different from the strongylar disease also met 
with in sbeep, to which the same name has been given, is obvious. 
It is not necessary to do more than point out that a pseudo- 
tuberculosis occurring specially in mice, has been described ; whilst 
Kutscher and Pfeiffer mention a form set up by the inoculation of 
material from glaudered horses. Pfeiflfer's bacillus is considered 
to be identical with Malassez and Yignars, and it is quite possible 
that Kutscher's is of the same nature. Hayem brought forward 
evidence that the human subject might be affected by the pseudo- 
tuberculosis bacillus (Tvhereulose zooglodque) a statement that is 
corroborated by the fact that Malassez and Yignal's pseudo- 
tuberculosis was induced by the inoculation of a guinea-pig with a 
portion of a nodule from a child that was said to be suffering from 

I believe that our President will bring before us to-night some 
interesting cases in which mechanical irritants have induced 
changes in the delicate tissues of tbe eye — changes which resemble 
very closely some of those met with in a true tubercular iritis. 
With these, however, he will deal, and it is necessary for me 
only to mention these mechanical irritants as producing changes 
somewhat similar to those that I have already described in the 
" Wurmknotchen " of the sheep. 

In comparatively recent times we have passed from the ana- 
tomical pseudo-tuberculosis to a pseudo-tubercle bacillus, a factor 
which promises, unless taken firmly in hand and in time, to render 
the question of pseudo-tuberculosis still more complicated. The 
smegma bacillus was comparatively easily dealt with so long as it 
was found only in certain well-defined positions, but Frau Babino- 
witcb opened a very serious question when, in milk and butter, 
she found a bacillus which, morphologically, and in its staining 
reactions, but in little else, was identical with tbe tubercle bacillus. 
Frau Rabinowitch's observations have been confirmed by other 
investigators, and we have now the two positions from which it is 

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absolutely necessary we should free ourselves by getting nd 
of terms which, under present conditions, can only end in inex- 
tricable confusion. On the one hand, we have pseudo-tubercle 
bacilli which have morphological and staining character of the 
true tubercle bacillus, but which pathologically appear to be 
widely separated from it; whilst, on the other hand, we have 
a whole series of lesions which present certain superficial re- 
semblances to tubercle in some of its forms, but which can be 
distinguished in most cases by certain specific differences, and, 
most important of all, are not induced by the action of the 
tubercle bacillus. One of the great difficulties that the earlier 
pathologists experienced in arriving at a definite conception of the 
pathology of tubercle was its protean form, and even in the present 
day, now that tuberculosis has come to be so intimately associated 
with the ultimate etiological factor — the tubercle bacillus — the 
bacillus itself rather than the exact histological lesions has come to 
be looked upon as the essential determining factor in classification, 
and, although in tuberculosis a general sequence of changes may be 
observed, these may be so masked, and take place at such very 
different rates, and give rise to such varying results, that it would 
be difficult to describe any single form of tubercle that should be 
taken as typical. When, therefore, it comes to be a question of 
comparing other pathological conditions, and speaking of them as 
pseudo-tuberculosis, it is necessary, if the term is to convey any 
distinct meaning to those to whom the process is being named and 
described, to give a kind of tuberculosis with which the pseudo- 
form is to be compared. For instance, what possible resemblance 
can there be between the pseudo- tuberculosis set up by Strongylus 
filarise in the sheep and the pseudo-tuberculosis of which I have 
thrown examples on the screen, the form occurring in guinea-pigs 
as the result of the action of the short polar-stained bacillus ? It 
is impossible to make out even a naked-eye resemblance ; whilst, 
when we come to the histological features and the pathological 
factors, any points of resemblance are absolutely wanting. In the 
same way the pgetfdo-tuberculoats ovis of Preisz is absolutely 
distinct from the filarial pseudo-ttiberctUoeis ovia ; whilst, coming 
to birds, the pseudo-tuberculosis described by Malassez and Vignal^ 
Nocard, Pfeiffer, Muir, and others is essentially different from 
the aspergillar tuberculosis also met with in birds; whilst the 
similar condition in man should no more be called an aspergillar 

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pseudo-tuberculosis than should a case of actinomycosis be said to 
be of a pseudo-tubercular nature. 

When we come to the histological features of tubercle, they are 
so varied at different stages and under different conditions that 
almost every new tissue at some period of its development may be 
said to be like some stage of a tubercular process : we find similar 
cells in the glanders nodule. Take the rapid infiltration of leuco- 
cytes, this also is met with in certain other specific conditions. 
Even the giant-cells, which are supposed to be so characteristic of 
chronic tubercle, may be mimicked, imperfectly no doubt, in 
ordinary granulation tissue and in the new tissue of the glanders 
nodule. The various forms of phagocytic cells met with in 
tubercle are, as might be expected, to be found in actinomycosis, 
in aspergillar pneumonomycosis, and, in fact, in all those conditions 
in which foreign bodies are to be absorbed, and iu which, too, 
irritant substances are produced by the action of the higher fungi 
or bacteria. 

Coming now to more general changes, one finds that endarteritis 
obliterans, taking this as an example, may be met with in tubercu- 
losis, in actinomycosis, in glanders, and in a variety of other con- 
ditions in which poisonous products are being developed regularly 
and over considerable periods of time; and in tubercle as in 
specific disease the caseation which results, although due no doubt 
in a certain measure to the direct action of toxic products, is the 
result also to some extent of the cutting off of the blood supply 
from the caseating area, brought about by the gradual obliteration 
of the blood-vessels. It seemed possible at one time that we 
should be able to simplify pathological nomenclature by gradually 
eliminating from the term tuberculosis all those conditions that 
are not brought about directly by the action of the tubercle 
bacillus A large number of conditions which had hitherto not 
been I'ecognised as tubercular were, in comparative pathology, 
brought into their proper position. For example, the term lymph- 
adenoma as applied to certain conditions met with in the horse in 
th6 spleen, in the mesentery and even in the lungs, has now been 
practically obliterated, as, owing to the investigations of McFadyean 
in this country, and Nocard, Ostertag, and others abroad, most of 
these lesions have been found to be typically tubercular ; whilst 
certain lesions in the cat and other feline animals, which have 
been described as glanders and caseous pneumonia, have also been 

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recognised as being tubercular, and it appears to me to be very 
inadvisable that we should, just as order is being evolved from 
chaos, bring in any nomenclature which can only ultimately lead 
to confusion ; and I hope to-night to have an expression of opinion 
on this point not only from those who take part in the discussion 
and exhibit specimens of what have hitherto been called '' pseudo- 
tuberculosis ;" but a suggestion from our President as to the best 
means of drawing up an accurate descriptive nomenclature of 
many of these forms of disease which at present are practically 

Pseudo-tuberculosis as a pathological entity has now no longer 
any existence, and, although it may be necessary, owing to the 
exigencies of use and wont, to retain the term tuberculosis, that 
term should be restricted as far as possible to a process which has 
a distinct etiological factor, and we should minimise, as much as 
possible, the evil of the term by eliminating altogether the term 

Dr. Sidney Martin said that in the course of time, when the 
conditions which were at present described under the name of 
pseudo-tuberculosis had been more completely studied, the name 
would have to be given up. Tuberculosis was a definite disease, 
caused by a well-known micro-organism, and the nodules (miliary 
tubercle) which constituted the early lesions of this bacillus under- 
went certain degenerate and other changes, such as caseation and 
peripheral fibrosis. Other living agents, as was now known, could 
produce appearances which were more or less similar to the naked 
eye and to microscopical examination. Dr. Martin was familiar 
with the lesions in guinea-pigs and rabbits which Dr. Sims Wood- 
head had referred to. These lesions were found in the liver, 
spleen, lungs, intestines, and mesenteric glands of many of these 
animals which were kept in large quantities for experimental pur- 
poses. The lesions consisted of whitish or whitish-yellow nodules, 
sometimes soft, sometimes hard, varying in size and shape and 
tending to coalesce ; microscopically they consisted of cells in 
varying degree of necrosis, and there was also found in the 
necrosed area, sometimes chiefly in the vessels round, groups of 
bacilli or of cocci to which the condition must be ascribed. No 
tubercle bacilli are found in these lesions. The lesions are best 
referred to as " bacterial necrosis," at any rate provisionally, until 

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the cbaracteristics of the micro-organisms producing them are 
more clearly known. To what extent these cases of slowly forming 
bacterial necrosis occur in man is not known. But there are 
other lesions produced by fungi which are becoming of great 
importance in the pathology of infective disease. Apart from 
actinomycosis, our knowledge of which is rapidly extending, there 
are lesions sometimes sufficient to cause death, and produced by 
fungi allied to the actinomyces, and which are called streptotbrix. 
Simon Flexner, in a recent article, refers to these diseased condi- 
tions as pseudo'tiiberculosis hominis streptothricha, and relates the 
case of a male negro, aged seventy, who was admitted to the 
hospital with the history of a chronic illness, and the symptoms 
and signs, among other things, of consolidation of the lungs. 
At the post-mortem examination, the upper lobe of the left lung 
was solid, grey, opaque, and softening; in the lower lobe there 
were scattered masses of consolidation. The middle lobe of the 
right lung was solid, and there were nodules in the rest of the 
lung, some calcified, some caseous. The omentum was thickened 
and rolled up, and showed lai^e and small nodules like those of 
tuberculosis ; these were also present in the liver and spleen. 

Histologically the nodules were composed of cells undergoing 
caseation and fibrin. Although no cultivation was obtained from 
the nodules, and the single inoculation experiment was practically 
negative, streptotbrix forms were present in the lesions of the 
lungs but not in those in the abdomen ; no tubercle bacilli were 
found. The case is incomplete, but it is a contribution to the study 
of chronic and caseating non-tuberculous disease of the lungs, and 
indicates the importance of looking out for such cases. Buchholz 
has described a case of mixed infection of the lung by streptotbrix 
and streptococcus; there was consolidation, excavation, and 
empyema. Scheele and Petruscky have described a case of infection 
by a hyphal fungus, in which the skin as well as the lung was 
affected. Other cases have been published under the name of 
"aspergillosis.** The subject, therefore, is at present very in- 
complete; but it is evident that, although the most common 
cause of caseating and destructive disease of the lungs (more 
particularly) is tuberculosis, yet there are other similar conditions 
produced by hyphal fungi. The mycelium of these fungi are not 
stained by the carbol-fuchsin method for tubercle bacilli, and 
Flexner makes the suggestion that in doubtful cases of lung disease 

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84j4j discussion on pseudo-tuberculosis. 

in which no tubercle bacilli are found in the sputum, it would be 
well to stain this by the Gram-Weigert method. 

Dr. Washboubn said that it would be advisable to discard the 
term pseudo-tuberculosis, as it was somewhat misleading. There 
were several bacilli which resembled the tubercle bacillus in 
morphology and in staining reactions. By some observers such 
bacilli would be called pseudo-tubercle bacilli. Tbey were of im- 
portance from the point of view of clinical diagnosis, for by relying 
upon a microscopical examination alone they might easily be mis- 
taken for the tubercle bacillus. In the urine pseudo-tubercle 
bacilli of this nature were by no means uncommon. It was on this 
account that inoculations were necessary for the diagnosis of tuber- 
culosis of tbe gonito-urinary tract. The term pseudo-tuberculosis 
was usually applied in quite a different sense to the above. It was 
used to denote diseases which resembled tuberculosis in morbid 
anatomy, but which were caused by other organisms than tbe 
tubercle bacillus. Of late a large number of such diseases had 
been described. There were many organisms which produced 
similar anatomical lesions to those produced by the tubercle 
bacillus. These organisms were of widely different character. 
There were bacilli such as the bacillus pseudo-tuberculosis, giving 
rise to caseating tubercles in many animals ; the bacillus pseudo- 
tuberculosis murium, causing caseating tubercles in mice ; and the 
bacillus pseudo-tuberculosis liquefaciens, causing tubercles in tbe 
peritoneum in the human subject and similar lesions in rabbits. 
There were various kinds of streptothrix, such as the one described 
by Flexner in the human lung. There were also organisms which 
do not belong to the class of bacteria ; a form of mould, the 
aspergillus, had been described as causing a tuberculous lesion 
in the human lungs ; an organism belonging to tbe class of the 
blastoniyces was described by Gilchrist and Stokes as producing a 
lesion resembling lupus vulgaris in the human skin; while even 
nematode worms might produce tubercles consisting of giant cells 
and epithelial cells in the lungs of cats and the kidneys of dogs. 
The skin disease described by Gilchrist and Stokes was of especial 
interest. Although it resembled lupus vulgaris in its clinical aspect, 
it was caused, not by the tubercle bacillus, but by a blastomyces, 
which they obtained in pure cultivations, and which when inoculated 
produced in animals tubercles consisting of epithelial cells and 

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giant cells. It was quite probable that many of the cases of so- 
called tuberculosis of the skin were due to other organisms than 
the tubercle bacillus. The speaker had seen such a case lately, in 
which tubercle bacilli could not be obtained either by microscopical 
examination or by inoculation. It was quite clear that the lesious 
caused by the tubercle bacillus were by no means specific, for many 
organisms might produce exactly the same changes. Again, the 
lesions produced by the tubercle bacillus were not constant ; some- 
times there was much caseation with formation of giaut cells, 
while in other cases there was the production of a granulomatous 
tissue. In fact, the tubercle bacillus and the other pathogenic 
oi^nisms mentioned obeyed a general law. They set up a more 
or less chronic form of inflammation, the character of which de- 
pended pai-tly upon the virulence of the organism and partly upon 
the relative susceptibility of the animal. Thus the same patho- 
genic organism might produce several types of inflammation, and 
the same type of inflammation might be produced by several 
pathogenic organisms. The most important lesson to be learnt 
from this discussion is the impoitance of making a systematic 
bacteriological examination of every case in the post-mortem room. 
The speaker was afraid that such a procedure was very much 
neglected, and he did not know of any post-mortem room in London 
where an adequate examination was conducted in every case. 

Br. Galloway said that he was glad that the subject of pseudo- 
tuberculosis had been brought forward, as it might give the oppor- 
tunity of disposing of a term which would inevitably lead to a 
confusion in our terminology if it were perpetuated. He noted 
with satisfaction that Dr. Woodhead and Br. Martin agreed on 
this point. There was little doubt that there are many specific 
granulomata causally associated with different micro-organisms 
which produced lesions in the form of tubercles, more or less 
resembling both in naked-eye and histological structure the 
lesions of what we understand as true tuberculosis. He imagined 
that it was too late in the day to use the word " tuberculosis *' as 
the designation for this group of diseases, and that we should still 
have to confine the name ** tuberculosis'* to the malady associated 
with Koch's bacillus tuberculosis. There would necessarily, there- 
fore, come about a revival in the use of the term "infective 
granuloma " to connote this group of disease. He hoped that we 

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should not have a repetition of such terminology as that used by 
Br. Flexner, of Baltimore, as a title to his important paper on 
the form of disease which he describes as " pseudo-tuberculosis 
hominis streptothricha.'* He considered that one of the results of 
Br. Flexner's paper would be to draw the attention of pathologists 
to the fact that the organisms of the streptothrix family were 
capable of producing other forms of disease than those already re- 
cognised under the titles of actinomycosis and madura foot disease. 
He remarked that he considered the present was a favourable 
opportunity of bringing under discussion any forms of disease in 
the human subject resembling tuberculosis, but probably unasso- 
ciated with Koch's bacillus tuberculosis. Eecently he had had the 
opportunity of studying two forms of cutaneous lesions which 
might well be placed in this category. 

1st. An example of a very characteristic form of granuloma 
occurring as a rule on the cutaneous surface of the lower eyelid, _ 
pursuing a chronic course, becoming finally absorbed, and some- 
times accompanied by the occurrence of similar small tumours on 
the face. A histological examination recently conducted on such 
a tumour from the lower eyelid revealed a structure not unlike 
tuberculosis in its general arrangement. There was a readily re- 
cognisable focus of round cell infiltration, mainly of leucocytes, the 
central part of which underwent a peculiar form of necrosis; 
caseation did not occur, but the connective- tissue elements and the 
cells seemed to pass into a condition of " mucoid '* degeneration 
previous to their absorption. Round the margin of this area of 
infiltration (especially the cutaneous margin) occurred numerous 
sharply-defined giant-cells. These giant,cells had numerous 
nuclei, usually peripherally arranged, and showing some dif- 
ferences, such as their regular contour and the exact distribution 
of their nuclei from the ordinary giant-cells of tuberculosis. In 
this particular instance he had examined numerous sections stained 
to demonstrate the presence of the bacillus tuberculosis with a 
completely negative result. Unfortunately, no material could be 
obtained for experimental inoculation, so that evidence from this 
source was not forthcoming. The rarity of diseases such as this 
makes a complete investigation difficult to make. He believed, 
however, that this form of disease was one that had been described 
as a giant-cell xanthoma of the eyelid, although none of the fatty 
material of true xanthoma is pi'esent. 

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2nd. Another example of a form of tumour wbich may come 
under this category had been brought to his notice by Br. 
Bade] iff e Crocker. In this case there appeared rapidly occurring 
nodular tumours of the skin, very closely resembling sarcomata. 
These tumours appear to be almost always multiple. Upon micro- 
scopic examination they were found to contain enormous numbers 
of giant-cells and undoubtedly presented close histological resem- 
blances to giant-celled sarcomata, but these tumours underwent 
spontaneous involution, so that their clinical course was very 
different from true sarcomata. 

Br. GkiUoway wished simply to allude to these two forms of 
disease so that they should be borne in mind in investigation of 
the forms of growth resembling tuberculosis. He felt sure that 
one of the results of the discussion of this evening would be 
greater care in the diagnosis of tubercular structures. Every one 
admits that the occurrence of giant-cells and even the appearance 
of *' giant-cell systems" such as have been described as diagnostic 
features of the tuberculosis of Koch are not sufficient to form an 
accurate diagnosis of the nature of the disease. The isolation of 
the associated micro-organisms, and especially the evidence obtained 
from experimental inoculation must become of supreme value. 
Judging from his slight experience, be considered that much light 
on the subject of the uncommon infective granulomata would be 
obtainable from the more careful study of the new forms of this 
class of disease observed in the tropics. 

Professor McFadyeaji said that the term pseudo- tuberculosis 
was open to the very serious objection that it could not be em- 
ployed in practice in strict conformity with any definition of it that 
could be framed. Adopting the widest definition possible, one 
might agree to include under the term all diseases other than that 
caused by Koch's bacillus, with lesions in the form of tubercles or 
nodules. But to any proposal to employ the term in this sense it 
might be objected in the first place that there was no need of a 
name for the heterogeneous affections which this would group to- 
gether, and in the second place that several diseases etiologically 
distinct from tuberculosis, and already provided with names irre- 
vocably fixed by long custom, had their most characteristic lesions 
in the form of tubercles. In glanders, for example, much more 
constantly than in tuberculosis, the primary lesions had the form 

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of tubercles, but no good purpose would be served by calling 
glanders a pseudo-tuberculosis. It would be absurd to call every 
disease other than tuberculosis with tubercle-like lesious pseudo- 
tuberculosis, and as a matter of fact the term had never been so 
employed. As far as one could trace any rule, in its application, it 
appeared to have been generally reserved for anatomically tuber- 
culous diseases that were until recently of obscure origin, and 
which, but for Koch's discovery, or the application of bacteriological 
methods of diagnosis, might still have been confounded with true 
tuberculosis. For each such case a new name had to be invented, 
but if pseudo-tuberculosis were the name chosen for the first case 
of the kind it thereby acquired a new meaning (just as tubercu- 
losis did after Koch's discovery of the specific bacillus) and must 
be reserved for that one disease. Unfortunately, however, it had 
already been applied in this way to several different diseases, and 
some degree of confusion was the inevitable result. He was in- 
clined to think that it would be better in the future to discard the 
tei-m altogether. With reference to the question of jposUmortem 
diagnosis of true tuberculosis, he thought that within the same 
species, the ox, for example, the appearance of the lesions was so 
characteristic as to leave little room for error in the case of persons 
of experience. The demonstration of tubercle bacilli might appear 
to be theoretically desirable in every case, but in slaughter- 
house inspection it was not practicable, and if insisted upon 
it would greatly increase the proportion of errors, owing to the 
occasional difficulty or impossibility of finding tubercle bacilli 
with the microscope in undoubtedly tuberculous lesions. On the 
other hand examination of the histology of the lesions was gener- 
ally sufficient to establish a diagnosis in tuberculosis of the horse, 
ox, and pig. Like some other observers, he had met with bacilli 
which might have been mistaken for tubercle bacilli owing to their 
staining reactions, but any such bacilli that he had encountered 
were morphologically different from the tubercle bacillus. 

In conclusion, he described (with lantern illustrations) a number 
of lesions of the lower animals which he found were pretty fre- 
quently mistaken for tuberculosis. 

Mr. Alexandbe Foulerton. — My object in taking part in this 
discussion was principally to protest against any use of the term 
"pseudo-tuberculosis." All this has, however, been done so 

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explicitly by Professor Sims Woodhead and most of those who 
have followed him, that it is unnecessary to add anything to what 
has already been said on that point. But, although the term pseudo- 
tuberculosis appears to be rightly discredited, it would seem that 
the fallacy upon which its use was founded is still, to a certain 
extent, prevalent. This fallacy is the supposition that there is 
anything anatomically characteristic about the tubercles which are 
found in the particular disease caused by the tubercle bacillus of 
Koch, and known as tuberculosis. I believe, on the other hand, 
that a tubercle is merely a common result of the action on the 
tissues of a large number of vegetable parasites, of which the 
bacillus of Koch is only one. And just as we do not speak of the 
abscess produced by one particular micro-organism as a "true" 
abscess, and of that produced by another micro-organism as a 
" pseudo "-abscess, so there is no reason for calling the tubercle 
produced by one parasite a true tubercle, and that produced by 
another parasite a pseudo-tubercle. And, further, I believe that it 
is impossible in the present state of our knowledge to distinguish 
with any measure of certainty by either anatomical or purely 
histological appearances between the tubercles produced by various 
different species of micro-organisms. Thus one might place side 
by side lungs containing grey miliary tubercles caused respectively 
by the bacillus of Koch, by the glanders bacillus, and by Aspergillus 
fumigatusy and I venture to assert that it would be impossible to 
say, from the anatomical appearances alone, which set of lesions 
were caused by each parasite. One would have first to identify the 
parasite itself. And with reference to this view of the matter I quite 
agree with what Br. Washbourn said as to the frequent inadequacy 
of the pathological examination of the bodies of those who have 
died with what has, on clinical grounds only, been diagnosed as 
tuberculosis. The pathologist is too often satisfied with a mere 
naked-eye inspection of certain anatomical changes before con- 
firming the clinical diagnosis, and this kind of confirmation 
appears to me to be of but little value. Bacteriology is an exact 
science, aud tuberculosis cannot now be regarded as the disease 
characterised by tubercles — for we know that there are many such — 
but as a disease due to infection by a specific parasite, the bacillus 
of Koch ; and the pathologist is not justified in describing a case 
as being one of tuberculosis, unless the causative parasite has been 
positively identified. In illustration of my contention I may refer 

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to a remark made during this discussion by a member who said 
that aspergillosis must be uncommon because he had never seen a 
case of pulmonary phthisis which there was any reason, anatomical 
or clinical, for supposing was not caused by the tubercle bacillus. 
Now, aspergillosis is probably a fairly uncommon disease in man, 
but it seems certain that when a pulmonary aspergillosis does occur 
it may be just one of those conditions which cannot be distinguished 
from pulmonary tuberculosis by either anatomical appearances or 
clinical symptoms. Aspergillosis is a disease which has been care- 
fully studied in France, especially since attention was called to the 
pathogenic action of Aspergillus fumigatiis, in a paper by Dieulafoy, 
Chantemesse, and Widal, read at the Berlin Congress in 1890. 
E^non and Lucet in particular have added much to our knowledge 
of the disease, the former having carefully described several cases 
of pulmonary aspergillosis in man, and the latter having given a 
very complete account of the infections by Aspergillus fumigatus as 
they occur in the lower animals. And, to repeat myself, it is quite 
clear that cases of pulmonary aspergillosis in man sometimes cannot 
be distinguished from pulmonary tuberculosis, either by the sym- 
ptoms occurring during life, or by the anatomical character of the 
lesions found after death. And the same remark applies to pul- 
monary aspergillosis in the cow and other animals. From my own 
observations I can say that grey miliary tubercles resulting in the 
lungs of a rabbit after an intravenous injection of a culture of 
Aspergillus fumigatus, are anatomically indistinguishable from those 
which one may get after an intravenous injection of the tubercle 
bacillus in the same species. The distinction between the two 
conditions is, of course, easily made by bacteriological methods. 
With regard to what have been called pseudo-tubercle bacilli, I do 
not think that they can be very common. The smegma bacillus, 
after the usual staining with carbol-fuchsin and treatment with 
83 per cent, nitric acid, is decolourised if the counter-staining is done 
with a solution of methylene blue in absolute alcohol. There are 
sometimes found in milk bacilli which, as Professor John McFadyean 
pointed out, resist the ordinary methods of decolourisation after 
staining with warm carbol-fuchsin, but which do not appear to be 
the tubercle bacillus of Koch. And these bacilli should be submitted 
to culture and inoculation tests before any opinion is given as to 
their nature. Before concluding I would like to briefly refer to the 
question of yeast infections. The pathogenic yeasts are of some 

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Illustrating Mr. Foulerton's remarks in Discussion on Pseudo- 

Fio. 1. — Tnmoiir in popliteal space and posterior tibial region of a rabbit 
after inoculation with a pathogenic yeast {Saccharomyeet tumefaciens alhus). 
About half natural size. 

Fig. 2. — Section through a similar tumour formed at site of inoculation in 
another rabbit. ( x 600.) 

Fig. 8. — Another portion of the same section as the last ( x 600.) Stained 
with methylene blue. 

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• I 'I vi,..,:..r ill' 

'iir fti^ai hI at ^iu* ol Ih*- » n' iTaii in 

'111.' Krt'''^":i' l-'.t I'l^f. ^v f\ 

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Path. Soc. Trans. Vol. L. Pl. XI. 

Fig. 1. 

Fig. 2. 

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Fig. 3. 

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Path. Soc. Trans. Vol. L. Pl. XII. 

Fig. 1. 


Fig. 2. 

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Fig. 3. 

tul""-«'l,ir 'V. 

liver f •-!.',. » t'l," I i* »»• it -t 

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niustrating Mr. Eoulerton's remarks in Discussion on Pseudo- 

Fig. 1. — Section through nodule on diaphragm of rahbit after inoculation 
with pathogenic yeast. ( x 20.) 

Fig. 2. — Section through same nodule on diaphragm. ( x 600.) 

Fig. 3. — Photog^ph of living* culture of S. tumqfaciens albus. From sub- 
culture, twenty-four hours old, on glucose agar, direct from secondary nodule in 
liver from same rabbit as last. 

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interest in connection with the present discussion because tliej are 
capable of producing tubercles which are indistinguishable anatomi- 
cally or histologically from tubercles produced by other vegetable 
parasites. I may perhaps also claim that the particular specimens 
which [Pis. XI, Xn] I am showing to-night have a further interest 
as being the first specimens of yeast infection which have been shown 
as such in this country. The first specimen can only be described 
as being probably a result of yeast infection, since, although it was 
thought that yeast cells could be identified in fresh ^* teased out " 
preparations, all attempts to isolate the veast by culture failed. 
The specimen consists of a portion of the rump muscles of an ox, 
and shows a number of round white nodules, which have the 
structure of granulomata. I believe that the case is in its nature 
similar to the disease which Prof. Tokishige has described as being 
commonly found in cattle and horses in Japan, where it is known 
as ** worms." Tokishige has practically proved that the disease is 
a blastomycetic infection. 

The other specimens and sections shown under the microscope 
are all the result of experimental inoculations with a pathogenic 
yeast (Saccharomyces tumefaciens aXbvs), and I may just mention 
that quite similar results may be obtained with a number of other 
species of blastomycetes. The first of these specimens consists of 
the lungs of one of three white rats, each of which received a small 
subcutaneous injection of this yeast. The animals died at intervals 
of three weeks, five months, and six months after the inoculation, 
and all presented a number of yellowish caseous nodules in their 
lungs after death. These particular lungs came from the rat 
which died at the end of six months, and are extensively infiltrated 
with the caseous nodules. These changes, again, can only be said 
to be probably due to the yeast infection, as I was not able to 
identify the yeast cells in the tissues. The next specimen shows 
a largish, firm, nodulated tumour in a rabbit, partly projecting 
into the popliteal space and partly embedded in the posterior 
tibial muscles. This tumour foiled at the site of inoculation, and 
the animal died on the fourteenth day. The tumour is a granu- 
loma, and from it a pure culture of the yeast was obtained. The 
remaining specimens came from a rabbit which died on the eighth 
day after a subcutaneous inoculation in the lumbar region. A 
tumour developed at the site of inoculation, and numerous tubercles 
were found in the lungs, liver, and kidneys, and scattered over the 

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diaphragm. The primary tumour and the secondary tubercles all 
presented the characters of granulomata. Cultures of the yeast 
inoculated were recovered from the primary tumour, from the 
tubercles iu the liver, kidneys, and diaphragm, and also from some 
urine which was found in the bladder. The first two slides show sec- 
tions through the primary tumour. In them numerous yeast-cells, 
many of which are " budding," can be seen. Some of the cells show 
an internal concentric arrangement of their contents, which reminds 
one of the similar arrangement described by San Felice and EoncaJi 
as occurring within the alleged yeasts found by them in carcino- 
mata. The next slide shows a section under a low magnification 
through one of the tubercles on the diaphragm. These tubercles 
were, except for the contained yeast, not to be distinguished from 
what one might have found in a case of tuberculosis. The next 
slide shows a section of the same tubercle under a higher power of 
the microscope. A large number of yeast cells can again be seen, 
many of which appear to be surrounded by a distinct capsule. A 
capsule, like the internal concentric arrangement, has also been 
described in connection with the alleged cancer yeasts. The next 
two lantern slides show photographs of cultures of the yeast grow- 
ing on glucose agar tubes inoculated from the primary tumour and 
from a tubercle of the liver. And the last slide shows a photo- 
graph of the living yeast cells from a culture obtained from the 

Mr. Pakes quite agreed with Prof. Sims Woodhead that the 
term pseudo-tuberculosis was one which should now fall into dis- 
use. A great amount of confusion always arose when the term 
pseudo was applied, as was evidenced by the pseudo-diphtheria 
bacillus. When, further, such conditions as pseudo-rickets, pseudo- 
erysipelas, and pseudo-leprosy were described the confusion became 
still worse. He thought that it would be preferable to attach a 
person's name to a condition until its pathology was determined 
rather than to tack the term pseudo on to a condition which merely 
bore a superficial resemblance to a condition whose pathology was 
known. The condition referred to by Prof. Woodhead as asper- 
gillo-pneumonomycosis was a very interesting one, and one which 
had been emancipated from its connection with tuberculosis. In 
this disease the pathological lesions very closely resembled those 
produced by the B. tuberculosis. The Aspergillus fumigatus could 

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cause lesions resembling both the acute and chronic lesions pro- 
duced by the B. tuherctUosis, He had come to the conclusion that 
there were more cases of aspergillosis than was generally imagined, 
and be suspected that some of the cases of supposed phthisis which 
recovered were possibly due to this cause. It was not very rare to 
find moulds in fresh sputum, and on more than one occasion he 
had been struck with tbe large number of these organisms. On 
one occasion he bad made cultivations, and found that the culture 
was an almost pure one of the Aspergillus fumigcUus. The obser- 
vation of Prof. Sidney Martin, that tubercle inoculated in, say, the 
groin of a guinea-pig was always followed by infection of the 
glands and lympb channels was, in his opinion, quite sufficient 
reason why tubercles found in the liver, omentum, &c., after inocu- 
lation without any chain of glands should not be called pseudo- 
tuberculosis. He had recently had such a case, which to the naked 
eye presented tubercles in the omentum. On section, however, 
small breaking-down cavities were found which contained a bacillus 
which stained easily with carbol- methylene blue. 

Dr. Lazabtjs-Bablow. — It is with great diffidence that I venture 
to put in a word for the retention of the term pseudo-tuberciilosis 
after I have heard the strong expressions of opinion for its aboli- 
tion that have fallen from the lips of the speakers who have pre- 
ceded me. And yet I think there is a certain number of cases in 
which use of the term may be distinctly advantageous. I suppose 
that its recognition is really a cause for self-congratulation rather 
than of reproach, a sign of knowledge rather than of ignorance. 
If we assume for the moment that the name " pseudo-tuberculosis " 
is to be retained, the question at once arises. To what class of case 
should it be applied ? It is quite clear that the purely anatomical 
conception of tubercle cannot be the criterion. Under that condi- 
tion we should be obliged, as Prof. McFaydean has said, to include 
glanders in the category, and besides that disease a host of others, 
such as actinomycosis, leprosy in certain forms, even cases of 
malignant disease where the manifestations are of the nodular 
type. Indeed, since the anatomical tubercle is simply the visible 
expression of a reaction on the part of the normal tissues of the 
body to an irritant of a certain degree of intensity, the term wo\ild 
become so wide and indefinite as to be quite useless. Quite ex- 
traneous conditions, too, might easily be brought into the group 


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" pseudo-tuberculosis " if the mere appearance were made the crite- 
rion. Thus, last week I had in the ijosi-moriem room an exquisite 
example of the confusion that would ensue if such a mode of de- 
fining pseudo-tuberculosis were adopted. The case was one in which 
there were minute emphysematous bullfle in the lung. They were 
the size of a millet seed, situated immediately beneath the pleura, 
raised so that they could be felt easily, firm and translucent. They 
were apparently typical " grey grantdations of tubercle." But when 
a section was made with a knife they, of course, collapsed and their 
nature was manifest. This case seems to me quite parallel with the 
case of verminif orm pseudo-tuberculosis mentioned by Prof. Wood- 
head. In both cases — and probably a very large number of other 
cases of so-called pseudo-tuberciilosis are subject to the same re- 
mark — a little extra knowledge or a little extra care completely 
severed them from tuberculosis, not because of their difference of 
appearance, but because of their difference in setiology. This brings 
us to the question whether the B. tvherculosia is to form the criterion. 
So far as concerns the actual recognition of what is tubercular, 
there can be no doubt that if the bacillus of tuberculosis is found 
we must undoubtedly pronoimce the lesion a tubercular one. It 
follows from this that a pseudo-tubercular lesion can only be either 
one which appears to be tubercular and is associated with a bacillus 
having the morphological and tinctorial properties of the tubercle 
bacillus but yet not the tubercle bacillus, or one which appears to 
be tubercular and is associated with no micro-organism at all so far 
as can at present be determined. Conditions which, however like 
tubercular lesions they may appear to the superficial observer, are 
nevertheless definitely associated with some parasite of whatever 
kind, I would call by distinctive names, however many were re- 
quired, but I would not speak of them collectively as examples of 
pseudo-tuberculosis. We have in ordinary life a somewhat similar 
example. We speak of a sovereign and of a counterfeit sovereign. 
The counterfeit sovereign must be so like the real coin that it will 
deceive the imwary and sometimes even the wary, but it must fail 
in the essential point : it is not made of gold. More than this, the 
counterfeit sovereign, if it is going to pursue its career of useful- 
ness, must rigidly withhold information — at least from the super- 
ficial or unskilled observer — as to the metal of which it is com- 
posed. So, I think, should be the case with pseudo-tuberculosis. 
It is not sufficient that a lesion should be anatomically and clini- 

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cally like tubercle ; it is not sufficient that it should not be caoised 
by the B. tuherculons ; it must rigidly withhold information as to 
its SBtiological factor. Directly it yields up that information I 
would have it referred to this category or that to which it legiti- 
mately belongs. It would be in the highest d^ree unscientific to 
term a condition " pseudo-tuberculous " when we have really good 
evidence that it is caused by some mould or animal parasite or 
other factor. And yet herein lies the weakness of the position. A 
very considerable number of the cases that have been grouped 
together under the name of pseudo-tuberculosis are cases in which 
some moiild or streptothrix is present in the tissues, and in which 
it is uncertain whether the micro-organism is causal or accidental. 
There is no inherent impossibility in the claim that a lesion re- 
sembling that caused by the B, tuberculosU may be caused by a 
parasite other than B. tuberculosis. There is no reason why the 
moiilds that have been found associated with lesions apparently 
tuberciilar should not really be causal ; that, for example, the case 
shoiild really be an aspergillosis, and not a tuberculosis at all. 
Until, however, the scientific proof is complete in these cases I do 
not know that I should greatly object to their being temporarily 
classed together as pseudo-tuberculoses. 

But there is one point on which I should lay very great stress. I 
am strongly of opinion that in a very large number of cases of so- 
called pseudo-tuberculosis, whether micro-organisms other than B. 
tuberculosis are obvious or not, a prolonged search would reveal 
the presence in the lesion of the true tubercle bacillus, and would 
therefore determine that the condition was not one of pseudo- 
tuberculosis but a true tuberculosis. There came under my notice 
last year a very pronoimced example in support of this statement. 
A cab-driver died in hospital after an illness of a few months in which 
pronounced wasting, severe night sweats, and troublesome cough 
with some expectoration were the most important symptoms. As 
was natural, it was diagnosed to be pulmonary tuberculosis. At the 
autopsy there was found pneumonic consolidation with a yellowish 
colour of the right lung from apex to base ; this consolidation was 
more advanced in the upper and middle lobes, where it was so con- 
siderable that portions of lung sank in water. There was not a 
great deal of excavation, but had the case lasted longer the degree 
of caseation was so great and the softness of the caseous material 
was such that the excavation would have proceeded by strides, and 

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the whole lung would have become converted in a short time into 
a huge vomica. As it was, there were numerous vomicse the size of 
a small pea, and filled with purulent material, and one or two the 
size of a bean. In the left lung anteriorly there was a small patch of 
consolidation of the same type. The clinical diagnosis was natur- 
ally confirmed by the macroscopic appearances of the lung. When, 
however, I came to examiae microscopical sections, I found that the 
" caseous pneumonia " was permeated by a strepto-bacillus of very 
definite appearance in all directions. This strepto-bacillus could 
not have gained access to the tissues after they reached my hands, 
for the material was preserved in strong spirit imtil it was ulti- 
mately embedded in paraffin, and since they were not confined to 
the surfaces but permeated the lung throughout, there is reason to 
believe that they were present in the body before death. As to the 
a<'tual part they played in causing the condition it is impossible to 
say, and for my present purpose it is immaterial. The case ob- 
viously assumed at the moment of their discovery a different com- 
plexion, and it became possible that it was one of pseudo-tubercu- 
losis and not one of true tuberculosis. I therefore prepared and 
stained by the Ziehl-Neelsen method with the greatest care over 
eighty sections of the material, in order, if possible, to determine 
the point. It was not till I reached the fiftieth section that I f oimd 
a single tubercle bacillus, but Id the fiftieth section I f oimd a region 
where B. tuberculosis was present in great numbers and was quite 
immistakable. I should have been absolutely wrong had I spoken 
of the condition as a pseudo-tuberculosis, and yet it required the 
examination to proceed far beyond the number of specimens 
ordinarily examined for the purpose before the diagnosis was cleared 
up. I cannot express my opinion in sufficiently strong terms that 
a similar result would follow in a large number of cases of ** pseudo- 
tuberculosis " if a sufficient number of sections were examined for 
tubercle bacilli. 

If, then, my opinion is that of cases of " pseudo-tuberculosis " a 
large number should be given places in definite categories, and that 
not a few are really cases of true tuberculosis, the question is why 
I should wish the term to be retained and what class of case I 
should include therein ? I think there is at present, and probably 
for some time there will remain, a residuum of cases upon which no 
other opinion can be pronoimced than that they are extremely like 
true tuberculosis and yet are in certain respects imlike it. For 

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these I would reserve the term. Thus I shoiild feel inclined to 
speak of the condition so frequently met with in the last stages of 
diabetes mellitus as a pseudo-tuberculosis when it is not definitely 
proved that it is a true tuberculosis, a matter often of extreme 
difficulty or impossibility. And other examples rise to one's mind ; 
I will grant that pseudo-tuberculosis is probably a term destined 
to vanish, but at all events at present I believe that it may be made 
to serve a useful purpose so long as its range is defined more 
strictly than has hitherto been the custom. 

Dr. Wbthbeed said that in 1891 he had the opportimity of inves- 
tigating "pseudo-tuberculosis," the material being obtained from 
two cultures sent from Paris of what was then known as the bacillus 
of pseudo-tuberculosis. At first there was some difficulty in obtaining 
pure ciiltures, but this was eventually accomplished by means of 
plate cultivations. The characteristics of the bacilli and colonies ' 
were the same as those already described by Dr. Sims Woodhead. 
The guinea-pigs inoculated died between the ninth and twelfth 
day. In every case an abscess formed at the site of inocula- 
tion. The animals inoculated from pure cultures showed small 
white nodiiles scattered through all the organs, which on naked- 
eye examination simulated the appearance seen in miliary tubercu- 
losis. Unless microscopic and bacteriological examinations had 
been made, the conclusion might very easily have been arrived at 
that the animal had died from tuberculosis. He agreed with the 
remarks made by Mr. Fakes as to the presence of aspergillus in 
the sputum of cases of supposed pulmonary tuberculosis. He had 
occasionally found the mould when diligent search failed to discover 
the tubercle bacillus. He echoed the remarks of previous speakers as 
to the desirability of doing away with the term pseudo-tuberculosis. 

Professor Woods Hutchinson. — I would like to call the atten- 
tion of the Society to a few specimens illustrating some of the forms 
of pseudo-tuberciilosis which I have collected in the past three 
months at the Zoological Gardens. One is an aspergillus ''tuber- 
culosis " of the lungs of a Trumpeter crane (Peophia crepitans) 
showing a number of brown masses of mould-growth just under 
the pleura. There were also several large plaques of mould upon a 
thick, cheesy basis in the air sacs of the bird. Another is a " worm- 
tuberculosis " of the lungs of a Capuchin monkey, in which the 

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coils of the worms can be clearly seen in the yellow nodnles with a 
hand-lens. Another is a probable yeast-tuberculosis of the lungs, 
liver, and kidneys of a prairie-dog, which, however, I have not yet 
had time to examine microscopically. The lung of a coyote studded 
with little, shotty nodules of bone, and the lungs of an agouti dotted 
all through with nodiiles and scars containing black pigments, are 
merely shown as imitations of some of the lesions usually associated 
with tubercle. 

The strongest impression made upon my mind by even my 
limited opportunities of study of these pseudo-tuberculoses is that 
they are an extremely heterogeneous and ill-assorted group. 
Almost their only connection with each other and with the great 
process whose "pseudo" name they bear, is that each of them 
resembles in some one or two points — often most crudely — true 
tuberculosis. Sometimes this resemblance consists solely in 
' the fact that tubercles, in the primitive sense of " little tubers," are 
produced, and the mind of the observer would needs be in a state 
of primseval innocence in order to even temporarily confuse them 
with the handiwork of the B, tuherculosis. 

Bearing in mind the three criteria, gross anatomy, microscopic 
appearance, and clinical history or systemic effects, there is not one 
of them (with the exception of some forms of the bacillary variety) 
which would conform to more than two of these tests and very few 
more than one. Microscopic examination will promptly distinguish 
all forms except the bacillary. Naked-eye appearances would 
easily disqualify all except the yeast, the bacillary, and a few forms 
of the mould varieties, and even the yeast and aspergillus nodes 
can be readily discriminated by a moderately expert eye. Only 
two varieties, the white aspergillus and the yeast resemble the 
** true " disease in their clinical history or systemic effects. I have 
seen the intestines of fat wethers in prime condition, killed in fact 
for export mutton, thickly studded with worm-tubercles, and the 
lungs and peritoneum of monkeys which had clearly died of other 
diseases, similarly affected. 

In short a thorough examination from all points of view reduces 
the danger of any of these ** pseudo " lesions being mistaken for 
true tuberculosis, to almost a " qucmtite nSgligeable.** 

Then why continue the use of the term pseudo-tuberculosis ? As 
already repeatedly stated, there is really no scientific ground for so 
doing, but, even at the risk of being considered reactionary, I should 

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like to say a few words in its favoiir, on the ground of practical 
convenience. The system of naming things or conditions by what 
they are not can hardly be endorsed on rational grounds, although 
it has one advantage, it leaves opportunity for the advance of our 
knowledge. We have only one chance in a thousand of being 
egregiously wrong. And there are not a few of our " positive " 
names which had better never have been applied, such as " ursemia," 
" pysBmia," ** melancholia," " epilepsy," ** lunacy." 

And yet imder the circumstances this term will probably continue 
to be used on account of its convenience. For it curiously so 
happens that the principal practical interest and importance of all 
these " pseudo " conditions centres in what they are not. From the 
point of view of the clinician, the veterinarian, the meat-inspector, 
if they are recognised as not tuberculosis, they may be practically 
disregarded. It matters little what they are, so far as prognosis is 
concerned, for, with the exception of the rare white aspergillosis and 
the yeast-tuberculosis, they give rise to no systemic infection or 
serious symptoms of any kind. To the pure pathologist, of course, 
the distinctions are of great importance, and he will find the use of 
such a " shot-gim " term as pseudo-tuberculosis a hindrance and dis- 
card it. But to the clinician it is of value to know that there are a 
rarity of conditions which simulate tuberculosis and yet have none 
of its fatal significance. And this clumsy term is really the only 
one which will cover this group. So widely do its members differ, 
that the only thing which unites them all is their liability to be 
mistaken for tuberculosis. Another practical difficulty in the way 
of getting rid of the term is the absence of a substitute. The 
group would have to be broken up into at least ten or fifteen 
different varieties, each having a new, strange, and terrible name, 
such as asjpergillosis, streptothricitis, saccharomycosis, <fec., which 
would convey no meaning whatever to the ear of other than an 
expert biologist. Instead of one foolish but easily understood 
name, we should have a dozen scientific but well nigh incompre- 
hensible ones. To continue an inept or even unfortimate term 
whose application is clearly understood, is often better than to 
change to a dozen new terms, more significant, it is true, but whose 
meaning future developments may also prove to be mistaken. Let 
it be clearly understood that pseudo- tuberculosis simply means any 
process which imitates the anatomical lesions of the B, tuherculoais, 
and its retention will not only be justifiable, but of much practical 

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value. It is perhaps no harm for us to be reminded, in these days 
of a rather too botanical pathology, that there are a number of 
oi^anisms and even agencies capable of exciting that swarm of 
angry leucocytes and new cells around an intruder which was 
known as the old "anatomical tubercle." And as all observers 
unanimously agree that 90 per cent, of all apparent " tuberculosis " 
are due to the action of the " genuine " bacillus, I think there is 
little danger of disturbing in any way the supremacy of the latter, 
or leading to any confusion in our now clear and definite concep- 
tions of the disease, by retaining the harmless " pseudo " term as a 
convenient designation for this insignificant minority. 

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The term "pseudo-tuberculosis" has been applied to several 
distinct morbid processes, which agree with one another only in 
the fact of producing in the tissues small nodular masses which 
have been considered to resemble " tubercles." 

Amongst the various morbid processes which have been so 
denominated are the following : 

(a) A number of bacterial infectione, caiised by bacilli and cocci of 

various species. 

As examples of such may be mentioned — 

1. A case of pseudo-tuberculosis in man, described by Bu Cazal 
and Yaillard (1891). In this case a number of caseous tubercles 
were found on the peritoneal membrane and in the pancreas. 
From these lesions a bacillus, differing from the tubercle bacillus 
of Koch, was isolated. This bacillus was not pathogenic for 
guinea-pigs, but produced in rabbits a condition comparable with 
that occuning in man. 

2. Zoogloea pseudo-tuberculosis of the guinea-pig and rabbit 
(" tuberculose zoogleique"). This condition was first described by 
Malassez and Yignal (1883) ; it resulted in the animals named 
after inoculation with portions of a nodule from the forearm of a 
child who had died with a tuberculous meningitis. The tubercle 
bacillus of Koch could not, however, be identified in the nodule 
in question. The first two series of rodents inoculated presented 
nodules in which a coccus with distinctive characters was found. 

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In the third series of inoculations the tubercle bacillus of Koch 
was found in addition to the characteristic coccus. The exact 
nature of the conditions in these particular cases must, therefore, 
remain doubtful. Chantemesse (1887) produced a zoogloea pseudo- 
tuberculosis of a similar kind in guinea-pigs by introducing into 
the peritoneum small portions of cotton wool through which had 
been filtered the air of a hospital ward iu which there were a 
number of phthisical patients. 

Nocard (1889), Zagari (1890), and Parietti (1890) described 
zoogloea pseudo-tuberculosis in the guinea-pig, occurring respec- 
tively after inoculation with the sputum of a cow which was 
suspected of tuberculosis, as a natural disease, and after inocula- 
tion with cow's milk. Eberth (1885) had also recorded two such 
cases occurring naturally in the guinea-pig. 

3. Zoogloea pseudo-tuberculosis of fowls, described by Nocard 

4. Bacillary pseudo-tuberculosis of rodents. Chan-in and Roger 
(1888), and Dor (1888), described this condition in the guinea- 
pig, and Eberth (1885) in the rabbit. Legrain (1891) described a 
similar condition occurring in the rabbit after inoculation with 
sputum from phthisical patients. 

5. Pseudo-tuberculosis of the ox. Courmont (1889) isolated 
from some nodules on the pleura of a cow a bacillus, differing from 
the tubercle bacillus of Koch, which produced a pseudo-tuberculosis 
in the guinea-pig. Nuvoletti (1894) has also described a bacillary 
pseudo-tuberculosis occurring in calves. 

6. Pseudo-tuberculosis of the horse, described by Pfeiffer 
(1889). The bacillus isolated produced a pseudo-tuberculosis in 
the hare, the rabbit, the guinea-pig, tame mice, and house mice. 

7. Pseudo-tuberculosis of mice, described by Kutscher (1889). 
This disease occurred naturally in some laboratory mice; the 
bacillus isolated was not pathogenic for either the guinea-pig or 

8. Pseudo-tuberculosis of sheep, described by Preisz and Gui- 
nard (1891). by Preisz and Morey (1893), and by Turski (1897) ; 
the bacillus isolated by these writers was pathogenic for both the 
rabbit and guinea-pig. 

9. Pseudo-tuberculosis of swine, described by Galli Valerio 
(1896). by Turni (1896), and by Deleidi (1896). 

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(h) Blastomycosis, 

Gilcbrist and Stokes have adopted a somewhat similar nomen- 
clature in describing a case of " pseudo-lupus vulgaris " caused by 
a blastomyces. 

(c) Streptotrichosis, 

Amongst streptothrix infections the following have been 
described : 

PseudO'tvherctdosis (cladothrica) by Eppinger. 

(Note.) — The fungus causing this disease was classed by 
Eppinger amongst the cladotriches ; it is now recognised as a 
streptothrix (S. asteroides). 

PseudO'tvherctdosis hominis streptotricha, by Flexner. 

{d) Aspergillosis. 

Infection by Aspergillus fumigatus was described as a pseudo- 
tuberculosis by Dieulafoy, Chant^messe, and Widal, and other 
authors have used the same term as descriptive of the pathological 
results of infection by certain mould fungi. 

(e) Protozoal infection, 

Gilchrist and Rixford have described a case of " Protozoan or 
Coccidioidal pseudo-tuberculosis." 

(/) Pathological conditions resulting from the presence of higher 
anim^ parasites in the luiigs. 

Hartenstein refers to a condition resulting from the presence of 
Echinococcus in the lungs of cattle as a pseudo-tuberculosis ; and 
nodules (" Wurm-Knotcben") brought about by the presence of the 
ova of Strongylus vasorum in the lungs of cats (Laulani6, 1884), 
and in the lungs of horses, cattle, sheep, and dogs by the ova or 
larv89 of nematode worms, have been described as ''verminous 


We think that confusion has arisen from the employment of the 
word ** tubercle" in two senses : 

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(1) As a general anatomical term for a small nodale. 

(2) In a specific sense for the nodular lesions of the disease 
produced by the tubercle bacillus of Koch. 


We think that the word should no longer be used as a general 
anatomical term ; but if used at all, it should be onlj as a designs* 
tion of the nodular lesions produced hy the tubercle bacillus. 

To prevent ambiguity, however, we suggest that all lesions 
having the form of "tubercles" should be called generally 
"nodules," those produced by Koch's bacillus being distin- 
guished as " tubercular nodules ;" and that the nodules produced 
by other causes should in like manner be distinguished by a 
prefix indicative of their cause, if known, — as, for example, " glan- 
ders nodule," " aspergillar nodule," or, if their cause is not known, 
by some distinctive designation not involving any reference to 
the word " tubercle." 

We further suggest that the diseases themselves (as distin- 
guished from the lesions produced) should, when possible, be 
designated in accordance with the plan indicated in headings (h), 
(c), and {d), "Blastomycosis," &c. 

• The term "pseudo-tuberculosis" would then become super- 
fluous, and ought in our opinion to be discarded altogether. 

J. F. Patne, Chairman, 
J. McFadtean. 
S. G. Shattock. 
J. W. Washbourn. 
G. Sims Woodhead. 
Alex. G. R. Foulbbton, Secretary. 
May 6th, 1899. 

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{For the list of Authors see p. 371.) 


ACHBOO-AMTLOID UYER, spleen, and kidneys (W. J. Hadley) . 134 

ACBOMEGALIC SKULL, and that of a normal giant (S. Q. Sbattock) . 185 

ACTIK0MTC08IS of the tongue (L. Cooper) . . .61 

ADEHOMA, multiple, in contracted kidney (F. P. Weber) . 179 

„ of breast^ associated with cyst and calcareous degeneration (C. F. 

Beadles) . . . . . . .228 

ADEHO-LIPOMA of submaxillary salivary gland (H. J. Waring) 67 

ADBENAL, cyst of (H. D. Kolleston) .214 

„ cystic disease of (B. Crawf urd) .... 212 

„ lesions of, in the insane (C. F. Beadles) .... 214 

AyjRMIA, pernicioas, peculiar condition of the colon in ; necrosis of the 

mucosa (H. M. Fletcher) . . . . .127 

„ splenic, with internal hsomorrhages, in infants (Q. B. Hunt) . 209 

AHEUKTSM of the splenic artery (H. D. Rolleston) . .56 

„ — (W. S. Lazarus-Barlow) . . . . .57 

AHTBUM, vacuolated, spheroidal-celled carcinoma of (H. D. Kolleston) . 251 

AOKTA, perforation of, by ulcer (probably syphilitic) of trachea (N. 

Dalton) . . . . . . .30 

APPENDIX YEBMIFOBMIS : See Vermiform appendix. 

ABTERIES, middle cerebral, embolism of ; rheumatic endocarditis ; carci- 
noma of the pancreas and liver (L. Freyberger) . .1 

ABTEKT, right common iliac, embolism of; incipient gangrene of leg; 

cardiac thrombosis, in typhoid (W. Hunter) . .52 

„ splenic, aneurysm of (H. D. Kolleston) . . .55 

„ — (W. S. Lazarns- Barlow) . . . . .57 

A8PEBGILL08I8 (?) of lung of horse (A. Q. K. Foulerton) . . 272 

ATSOPHT, symmetrical senile, of parietal bonei (H. M. Fletcher) . 195 

AUBICLE : See Heart. 

BILE-DUCTS, syphilitic stricture of (W. S. Lazarus-Barlow) . 158 

BILIABT CALCULUS : See Calculus, biliary. 

BLACX-WATEB, or hemoglobinuric fever (W. H. Crosse and W. C. C. 

Pfckes) . . . . . .273 

BLOOD-FILMS, the technique of ( W. C. C. Pukes and R. Howard) . 328 

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366 INDEX. 

BOHE, fhicture of cervical portion of spinal column (U. P. Potter) . 196 

BSACHIAL PLEXUS, fibroma of, associated with molluscum fibronnm (T. 

Carwardine) . . . . . .27 

BSEA8T, adenoma of, associated with cyst and calcnreoas degeneration 

(C. F. Beadles) . . . . .228 

„ "butter " cyst of (H. B. Robinson) . . . .227 

„ cystic disease of, in a boy (D'Arcy Power) . . 225 

BUVfY COAT, significance of, in the shed blood of acute pneumonia, etc. 

(S. G. Shattock) . . . . . .279 

CALCANEUM, central spindle-celled sarcoma of (P. de Santi) . 198 

CALCULI, biliary, healed perforation of duodenum after passage of (C. F. 

Beadles) . . . . . . .113 

CALCULUS, biliary, in children (G. F. Still) . .161 

CABCIB'OMA, columnar-celled, arising in remains of Meckel's diverticulum 

(?) at the umbilicus in an adult (C. D. Green) . . . 243 

„ cystic papilliferous ; sequel to a case of, arising in accessory thyroid 
(?), and leading to gland infection (A. E. Barker) . . 251 

„ squamous-celled, in substernal region (W. S. Lazarus-Barlow) 248 

„ vacuolated spheroidal-celled, of antrum (H. D. RoUeston) . . 249 

„ of stomach. See Stomach, 

CABDIA : See Stomach. 

CHBOMOCTTE CLUMPIKG in acute pneumonia and certain other diseases, 
and the significance of the huffy coat in the shed blood (S. G. 
Shattock) . . . . . . .279 

CIBBHOSIS, chronic, acute degeneration of liver-cells supervening in the 

course of (F. P. Weber) . . . . .186 

COLITIS, diffuse ulcerative, with secondary acute interstitial hepatitis (T. 

D. Lister) . . . . . .180 

C0L017, peculiar condition of (necrosis of mucosa), in pernicious anaemia 

(H.M.Fletcher) . . . . . .127 

COBD, spinal : See Spinal cord, 

CYST, "butter," of breast (H. B. Robinson). .227 

„ dermoid, multiple abdominal (A. C. Latham) . . 282 

„ multiple, in relation with an inguinal hernial sac in a woman (H. B. 

Robinson). ...... 230 

„ of the adrenal (H. D. RoUeston) . . .214 

CYSTIC DISEASE of breast in a boy (D'Arcy Power) . . .225 

„ of adrenal (R. Crawfurd) ..... 212 

DEFICIE17CT and redundancy of limbs, congenital (R. Barwell) . 819 

DERMOID CYSTS : See Cyst, dermoid. 

DEXTROCARDIA, left superior vena cava, endocarditis (N. Dal ton) 41 

DIABETES HELLITUS, atrophied pancreas from a case of (T. W. P. 

Lawrence) . . . . . .171 

„ sarcoma of pnncreas (T. Churton) .... 178 

DIARRH<EA. fatal summer, with acute enteritis, two cases, bacteriology of 

(F. W. Andrewes) . . . . . .118 

DILATATION of the right ventricle upwards and to the left (T. S. Wilson) 41 

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DIPHTHEBITIC PARALT8I8, further evidence on the pathology of (F. E. 

Batten) . . . . . . .22 

DUODEHAL ULCER from a case of melioDa neonatorum (T. D. Lister) . Ill 

DUODEBUM, healed perforation of, after passage of gall-stones (C. F. 

Beadles) . . . . . . .118 

EMBOLISM of both middle cerebral arteries; rheumatic endocarditis; 

carcinoma of the pancreas and liver (L. Freyberger) . 1 

„ of the right common iliac artery ; cardiac thrombosis in enteric fever ; 

incipient gangrene of leg, etc. (W. Hunter) . . .52 

EHDOCABDinS DEXTSOCASDIA, left superior vena cava (K. Dalton) 41 

EHTESOLITH from the rectum (S. G. Shnttock) . .134 

JCATI^HkLIAL tumours of skin, probably congenital in origin (nature 

ambiguous) (H. R. Crocker) ..... 220 

PAT NECROSIS, lesions of the pancreas with (C. F. Beadles) . 174 

FIBROMA from the neck of a child (congenital) (H. A. Lediard) . 223 

„ of bmchial plexus, associated with moUusonm fibrosum (T. Carwardine) 27 

FIBRO-SARCOMA, multiple, of scalp, of nineteen years' duration ; removal ; 

recurrence in lungs (P. de Santi) .... 234 

FRACTURE of cartilaginous portion of trachea ; fractures of sternum and 

ribs (W. S. Lazarus-Barlow) . . . . .32 

GALL-STOHES : See Calculus, biliary . 

GASTRIC, GASTRECTOMT, etc. : See Stomach, 

GERMICIDAL ACTIOIT, the relations of chemical composition to (J, 
Ritchie) ...... 

OIAJTT, skull of a normal, and an acromegalic skull (S. Q. Shattock) 
GLAND : See Breast, Pituitary, etc. 
GLIOMA of pineal body (T. W. P. Lawrence) 

HiEMOQLOBINURIA, or black-water fever (W. H. Crosse and W. C. C 
Pakes) ...... 

HEART, left auricle, extreme dilatation of, without mitral stenosis (H. M. 
Fletcher) ...... 

„ right ventricle, dilatation of, upwards and to the left (T. S. Wilson) 

„ spontaneous rupture, two cases of (C. F. Beadles) . 

„ thrombosis of lett ventricle in typhoid; embolism of the right 
common iliac artery; incipient gangrene of leg; infarcts in spleen 
and kidnevs (W. Hunter) .... 

HEPATITIS, acute interstltiul, secondary to diffuse ulcerative colitis (T. D, 
Lister) ...... 

HERNIA, cysts in relation with sac of an inguinal (H. B. Robinson) 

H7PERTR0PHT, congenital, of the pylorus; three ca^es, witli table of 
normal measurements (Q. F. Still) 
„ congenital, of pylorus (H. M. Fletcher) . 
„ idiopathic, of the oesophagns (H. D. RoUeston) 
„ of the right lung, obliteration of left (N. Dalton) . 








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368 INDEX. 


UrSAHE, lesions of the adrenal in the (C. F. Beadles) . 214 

IHTJfBTJLNE : See Colon, Rectum, 

nrrUSSUSCEPTIOir, two unusaal cases of (D'Arcy Power) .121 

EIDIIST, multiple adenomata in contracted (F. P. Weber) . 179 

„ small lipoma of ( P.P. Weber) . . . . . 181 

LDCBSf congenital deficiency and redundancy of ( R. Barwell) 319 

LIPOMA, a peculiar, of the groin (C. F. Beadles) .229 

„ of kidney (P. P. Weber) . . .181 

LIVEB, achroo-amyloid, spleen, and kidneys (W. J. Hadley) . 134 
„ cirrhosis, apparently due to congenital syphilis, with thrombosis of the 

hepatic veins (T. Churton) ..... 145 
„ cirrhosis of, probably syphilitic, assriciated with thrombosis of the 

hepatic yein (W. S. Lazarus-Barlow) .... 146 

„ condition of, in hepatic and portal thrombosis (H. D. Bolleston) . 148 
„ cysts in, containing living Param<zeia coli (A. £. Russell and E. F. 

Buzzard) . . . . . .149 

„ diffuse fibrosis of, in congenital syphilis (H. M. Fletcher) . 138 

„ diffuse syphilitic changes in (adult) (P. P. Weber) . . 142 

„ primary carcinoma of, spheroidal-celled (C. D. Green) . . 166 

.^ tuberculous cavities in (H. M. Fletcher) .... 160 

LIVES CELLS, acute degeneration of, supervening in the course of chronic 

cirrhosis (F. P. Weber) . . . , .136 

LUHG, hypertrophy of the right, obliteration of left (N. Dalton) . 33 

„ left, a case of sarcoma of, and of the mediastinum (C. D. Qreen) . 37 

MAMMA : See Breast, 

MECKEL'S DIVESTICULUM ; the source of a columnar-celled carcinoma 

(?) at the umbilicus, in an adult (C. D. Green) . . . 243 

M£L£NA 5E017AT0EUM, duodenal ulcer from a case of (T. D. Lister) . Ill 

MELAKOnC SAECOMA : See Sarcoma, melanotic. 

MOLLUSCUM FIBROSUM ; fibroma of brachial plexus associated with 

(T. Carwardine) . . . . . .27 

MTCOSIS, aspergillar (?) of horse's lung (A. G. R. Foulerton) . . 272 

MTOMA of oesophagus (H. D. RoUeston) .78 

„ of stomach (A. G. R. Foulerton) . .85 

„ of prostate, removed (T. Carwardine) .... 183 

MYXOMA from the thigh (H. D. RoUeston) . . .229 

MTXO-FIBRO-ADEHOMA arising in the region of a socia parotidis (H. D. 

RoUeston) . . . . . .66 

HECBOSIS, fat, lesions of the pancreas with (C. F. Beadles) . 174 

KEURO'FIBBOMA of brachial plexus associated with moliuscum fibro- 

sum (T. Carwardine) . • .27 

irODULE, rheumatic, the histology of (F. J. Poyuton and G. F. Still) . 324 

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INDEX. 369 


(ESOPHAaUS, fusiform dilatation of (W. S. Lazarus- Barlow) . 71 

„ hypertrophy, idiopathic, of (H. D. Rolleston) . . .69 

„ involved in spheroidal-celled carcinoma of the stomach (W. S. Lazarus- 
Barlow) . . . . . . .101 

„ myoma of the (H. D. RoUeston) . . . .73 

PAHCSEA8, atrophied; from a case of diabetes mellitus (T. VV. P. Law- 

D. Ro!les- 


„ columnar-celled carcinoma (primary) of the tail of the (H. 

ton) . . . . . . .171 

„ lesions of the, with fat necrosis (C. F. Beadles) . . .174 

„ sarcoma of; glycosuria (T. Churton) .... 178 

PAPILLOMA of rectum discharged spontaneously (T. Carwardine) 133 

PARALYSIS, diphtheritic, further evidence on the pathology of (F. E. 

Batten) . . . . . . .22 

PABAIKECIA COLI in hepatic cybts (A. E. Russell and E. F. Buzzard) . 149 

PARIETAL BONES, symmetrical senile atrophy of (H. M. Fletcher) . 195 

PEARLS, epithelial, in the tonsil (H. Walsliam) . . .65 

PERNICIOUS ANEMIA : See Anamia, perniciout, 

PINEAL BODT, cyst of (A. E. Garrod) . .14 

„ — two examples (A. E. Russell) . . . .15 

„ dilatation of central cavity of ; two examples (A. W. Campbell) . 15 

„ glioma of (T. W. P. Lawrence) . . . .12 

„ (1) sarcoma of, with diffused melanotic sarcoma of the surface of cere- 
brum ; (2) alveolar sarcoma of (C. Ogle) . . .4 
„ syphilitic disease of; general remarks on the pathology and normal 

structure of the (J. R. Lord) . . . . .18 

PITUITART GLAND, hypertrophy of, unassociated with acromegaly (J. and 

T. W. P. Lawrence) . . . . . .202 

PROSTATE, myomata of, and vesical calculus, removed from the same 

patient (T. Carwardine) ..... 183 

PSEUDO-TUBERCULOSIS, Discussion on, Introductory Address (Prof. 6. 

Sims Woodhead) . . . . . .331 

„ — (S. Martin) . . . . .342 

„ — (J. W. Washbourn) . . .344 

„ — (J. Galloway) . . . . . .345 

„ — (Prof. J. McFadyean) . . . . .347 

„ — (A. G. R. Foulerton) . . . . .348 

,, — (W. C. C. Pakes) . . . . . .352 

„ — (W. S. Lazarus-Barlow) . . . . .353 

,. ^ (F. J. Wethered) . . . . .357 

„ — (Prof. Woods Hutchinson) ..... 357 

„ report of committee upon the nomenclature of the conditions sometimes 
described as ..... . 361 

PTL0RU8 : See Stomach. 

RECTUM, enterolith from (S. G. Shattock) . . . .134 

„ villous papilloma of, discharged spontaneously (T. Carwardine) . 133 

RECURRENT LARYNGEAL NERVES, pressure on, by calcareous glands ; 

anthracosis of the lungs (N. Dalton) . . . * 31 


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370 INDEX. 


Green's case of umbilical papilloma in a woman let. 50 . . 247 

yy upon Mr. A. £. Barker's specimen of recurrent cystic disease, originally 

arising in the thyroid (?) . . . . . 254 

,, OF COMMITTEE upon the nomenclature of the conditions sometimes 

described as pseudo-tuberculosis .... 361 

RHEUMATIC NODULE, the histology of (F. J. Poynton and G. F. Still) . 324 

SARCOMA, giant-celled, of the neck (H. J. Waring) . . .232 

„ melanotic, with secondary growths of unusual size in the small intestine 

(H. C. Thomson) . . . . .237 

^ round-celled, involving the region of the pancreas, the adrt-nals, liver, 

and left lung (C. F. Beadles) . . . . .239 

„ round-celled, of pancreas ; diabetes mellitus (T. Churton) . . 178 

„ round-celled, of spinal cord, in a child (F. E. Batten) . . 21 

„ melanotic, of pineal body, with diffuse formation on surface of cerebrum 

(C.Ogle). . . . . . .4 

„ alveolar, of pineal body (C. Ogle) . .4 

„ spindle-celled, central, of calcaneam (P. de Santi) . . . 198 

SKIH, epithelial tumours of, probably congenital in origin (H. R. Crocker) 220 

SOCIA PAROTIDIS, myxo-abro-adenoma arising in tlie region of (H. D. 

Rolleston) . . . . . .66 

SPINAL COLUMN, crushed fracture of, in cervical region (H. P. Potter) . 196 

SPINAL CORD, sarcomata involving the, in a child ist. 3 years (F. E. 

Batten) . . . . . . .21 

SPLENIC AN£MIA with internal hemorrhages in infants (G. B. Hunt) . 209 

SPRUE, three cases of (J. H. Drysdale) . . . .114 

STOMACH, multiple erosion of the mucosa of (H. D. Rolleston) . . 73 

„ ulcer of, from a patient with chronic nephritis (H. D. Rolleston) . 75 

„ tubercular ulcer of, in children ; five cases (G. F. Still) . . 76 

„ tubercular ulceration of, in a child (T. D. Lister) . . . . 83 

„ pylorus, congenital hypertrophy of, three cases, with table of normal 

measurements (G. F. Still) . . . . .86 

„ (H. M. Fletcher) . . . . .98 

„ myoma of (A. G. R. Foulerton) . . . .85 

„ cardia, carcinoma of (H. D. Rolleston) . . . .99 

„ (A. F. Voelckcr) . . . . .100 

„ colloid carcinoma of (R. G. Hebb) .... 102 

„ spheroidal-celled carcinoma of, involving the (esophagus (W. S. Laxaros- 

Barlow) . . . . . . .101 

„ carcinoma developing in the scar of a gastric ulcer (H. R. B. Hickman) 109 
„ gastrectomy for carcinoma of; death forty hours afterwards ; infiltration 

of oesophagus (T. F. Chavasse) . . . .105 

SUBMAXILLARY SALIVART GLAND, adeno-lipoma of (H. J. Waring) . 67 

SUPPURATION of knee-joint, apparently aseptic ; phagocytosis of extrava- 

sated red blood-corpuscles by leucocytes (F. W. Andre wes) . . 199 

SUPRA-RENAL BODT: ^^ Adrenal, 

STPHILIS, cirrhosis of liver apparently due to congenital, with throm- 
bosis of the hepatic veins (T. Churton) .... 145 
„ congenital, diffuse infiltration of liver in (H. M. Fletcher) . 138 

„ diffuse change in liver (adult) (F. P. Weber) . . .142 

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STPHUITIC disease of the pineal body (J. R. Lord) . 
„ stricture of bile-dncts (W. S. Lazarus-Barlow) 

TESTICLE, an undescended left (A. P. Voelcker) 

THROMBOSIS of left ventricle; typhoid fever; embolism of the right 
common iliac artery, etc. (W. Hunter) . . . . 

„ of the hepatic veins; cirrhosis of liver apparently due to congenital 
syphilis (T. Churton) ..... 

„ of hepatic vein, associated with cirrhosis of the liver, probably 
syphilitic (W. S. Lazarus-Barlow) 

„ hepatic and portal, condition of liver in (H. D. Rolleston) . 

TONGUE, actindlnycosis of (L. Cooper) 
„ congenital cyst of the base of (R. Johnson) 

TONSIL, epithelial pearls in the (H. Walsham) 

TOXICITT of normal urine ; experiments upon (W. P. Herri ngham) 

TfiACHEA, transverse fracture of the cartilaginous i)ortion ; fractures of 
sternum and ribs (W. S. Lazarus-Barlow) 
„ ulcer (probably syphilitic) of, involving the left recurrent laryngeal 
nerve and perforating the aorta (N. Dalton) 
TUBESCUL08IS, congenital, in calves (J. McFadyean) 












TJN80UND MEAT, on infections caused by, more especially with regard to 

the BaciUus enteritidis (Gartner) (H. E. Durham) . . 262 

UEDTE, experiments upon the toxicity of normal (W. P. Herringham) 

VEINS, subcutaneous, an apparent thickening of (F. P. Weber) 
YENA CAVA, inferior, tuberculosis of (J. H. Drysdale) 
VENTRICLE: See Heart. 

VERMIFORM APPENDIX in which a pin had lodged ; no symptoms (H. A 
Lediard) ..•••• 





ANDREWES (P. W.), a case of apparently aseptic suppuration of the knee- 
joint, following injury, and associated with phagocytosis of extra vasated 
red blood-corpuscles by leucocytes . . • * lio 

, fatal summer diarrhcoa with acute enteritis . . .118 

BARKER (A. E), the final sequel to a case already reported, of recurrent 

cystic disease of a supposed accessory thyroid . • .251 

BARWELL (R.), a case of congenital limb deficiency and redundancy 
BATTEN (P. E.), ^further evidence on the pathology of diphtheritic para- 
lysis . . • • • • 

„ sarcomata involving the spinal cord of a child tet. three years 



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372 INDEX. 

BEADLES (C. P.)> adenoma of breast, associated with cyst and calcareous 

degeneration ...... 223 

„ a peculiar lipoma of the groin . . . . . 229 

„ healed perforation of duodenum after passage of g^ll-stones . .118 

„ lesion of the pancreas with fat necrosis .... 174 

„ round-celled sarcoma, involving the region of the pancreas, adrenals, 

liver, and left lung ...... 239 

„ some lesions of the adrenals in the insane . .214 

„ spontaneous ru]>ture of the heart . . . .49 

BUZZABD (£. P.) and RUSSELL (A. E.), cysts in the liver containing 

living Paramacia colt ..... 149 

CAMPBELL (A. W.), notes on two cases of dilatation of the central cavity 

of ventricle of the pineal gland . . .15 

CABWASDIlfE (T.), neuroma of brachial plexus, with molluscum fibrosum 

of skin . . . . . . .27 

„ prostatic myoma and vesical calculus removed from the same patient . 183 
„ villous papilloma of rectum ..... 133 

CHAVASSE (T. F.), a case of gastrectomy for carcinoma of the stomach . 106 
CHUSTON (T.), a case of cirrhosis of liver, apparently due to congenital 

syphilis, with thrombosis of the hepatic veins . 145 

„ sarcoma of pancreas ; glycosuria .... 178 

COOPEB (L.), actinomycosis of the tongue . .61 

CBAWPUBD (B.), cystic disease of the adrenal . . .212 

CROCKER (H. R.), epithelial tumours of the skin, probably of congenital 

origin ....... 220 

CROSSE (W. H.) and PARES (W. C. C.)> black-water, or lismoglobinuric 

fever ....... 273 

DALTON (S,), a case of pressure on the recurrent laryngeal nerves by 

calcareous glands, with anthracosis of the lungs . . .31 

„ dextrocardia ; left superior cava ; endocarditis . .41 

„ hypertrophy of the right lung, with obliteration of the left . . 33 

„ ulcer of the trachea involving the left recurrent laryngeal nerve, and 

perforating into the aorta . . . .30 

DRTSDALE (J. H.), three cases of sprue .... 114 
„ tuberculosis of the inferior vena cava . .60 

DURHAM (H. E.), on infections by unsound meat, more especially with 

regard to the Bacillus enleritidis (Gartner) . . 263 

FLETCHER (H. M.), congenital hypertrophy of the pylorus 98 

„ extreme dilatation of the left auricle without mitral stenosis 48 

-„ diffuse infiltration of the liver in congenital syphilis . 188 

„ peculiar condition of the colon in pernicious anaemia 127 

„ symmetrical senile atrophy of the parietal bones . . . 195 

„ tuberculous cavities in the liver .... igo 

FOULERTON (A. Qt. R.), myoma of the stomach .85 

„ mycosis (aspergillar P) of lung of horse . . . 272 

„ discussion on pseudo-tuberculosis .... 348 

„ report ot sub-committee on pseudo-tuberculosis . . . 861 

FRETBER6ER (L.), embolism of both middle cerebral arteries, rheumatic 

endocarditis, and carcinoma of the pancreas and liver . . 1 

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INDBX. 373 

GALLOWAT (J.), discoBsion on pseudo-tuberculosis 345 

GABROD (A. £.)> lung showing uniformly distributed fibrosis 36 

„ pineal cyst . . . . . . .14 

GBEEH (C. D.), a case of carcinoma of the liver, believed to have been 

primary ....... 166 

„ a case of sarcoma of left lung and mediastinum . . .37 

„ a case of umbilical papilloma in a woman set. 50^ apparently arising in 

remains of a MeckeFs diverticulum .... 243 

HADLET (W. J.), achroo-amyloid liver, spleen, and kidneys 134 

HEBB (B. 0.), a case of colloid carcinoma of the stomach 102 

HEBBnrGHAM (W. P.), experiments upon the toxicity of normal urine . 293 

.HICKMAK (H. B. B.), carcinoma developing in the cicatrix of a g^tric 

ulcer ....... 109 

HUNT (0. B.), two cases of splenic ansemia, with internal hsemorrhages, in 

infants ....... 209 

HUHTEB (W.), heart thrombus in a case of enteric fever ; embolism of the 
right common iliac artery ; gangrene of the leg ; infarcts in the spleen 
and kidney . . . . . .62 

JOHNSOH (B.), congenital cyst of the base of the tongue . 62 

LATHAM (A. C), multiple abdominal dermoids . . . 232 

LAWBEHCE (T. W. P.), atrophied pancreas from a case of diabetes mellitas 171 
„ tumour of the pineal body . . . . .12 

„ and (J.), hypertrophy of the pituitary body . . . 202 

LAZABUSBABLOW (W. S.), a case of substernal carcinoma . 248 

„ aneurysm of splenic artery . . . . .57 

„ discussion on pseudo- tuberculosis .... 353 

,, fusiform dilatation of the oesophagus . . . .71 

„ spheroidal-celled carcinoma of the stomach involving the cesophagus . 101 
„ syphilitic stricture of bile-ducts . . - . . 158 

„ thrombosis of hepatic vein associated with cirrhosis of tlie liver, 

probably syphilitic . . . . . .146 

„ transverse fracture of the cartilaginous portion of the trachea . 32 

LEDIABD (H. A.), appendix vermiformis in which a pin was lodged 126 

„ congenital fibroma from the neck of a child . . . 223 

LI8TEB (T. P.), a specimeu of tubercular ulceration of the stomach from 

a child . . . . . . .83 

„ a specimen of diffuse ulcerative colitis with secondary acute interstitial 

hepatitis ....... 130 

„ a specimen of duodenal ulcer from a case of melsena neonatorum 111 

LOBD (J. B.), the pineal gland : its structure; remarks on its pathology ; a 

case of syphilitic enlargement . . . .18 

MCFADTEAV (J.), congenital tuberculosis in calves . . 268 

„ discussion on pseudo-tuberculosis .... 347 

„ report of sub-committee on pseudo- tuberculosis . . . 361 

KABTIN (8.), discussion on pseudo-tuberculosis . 342 

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874 INDKX. 

OGLE (C.)> (1) sarcoma of pineal body, wifch diffused melanotic sarcoma of 

the surface of the cerebrum ; (2) tumour of pineal body in a boy . 4 

PAEES (W. C. C.) discussion on pseudo-tuberculosis . . 352 

„ and HOWARD (£.)> the technique of blood-films . . 328 

PATHE (J. F.), report of sub-committee on pseudo-tuberculosis . . 361 

POTTER (H. P.), crushed fracture of the cervical spine . 176 

POWER (D'ARCT), cystic disease of the breast in a boy ag^ three years . 225 
„ two unusual cases of intussusception .... 121 

POTVTOH (P. J.) and STILL (0. P.), the histology of the rheumatic 

nodule ....... 824 

RITCHIE (J.), the relations of chemical composition to germicidal action . 256 

ROBnrSOBr(H.B.)," butter "cyst of the breast . .227 

„ cysts in relation with the sac of an inguinal hernia . . 230 

ROLLESTOK (H. D.), aneurysm of the splenic artery . .55 

„ a tumour arising in the region of the socia parotidis . 66 

„ carcinoma of the cardiac orifice of the stomach . . .99 

„ cyst of the adrenal ...... 214 

„ gastric ulcer from a patient with granular kidneys . . . 75 

„ idiopathic hypertrophy of the ODsopbagus . . .69 

„ large myxoma of the thigh ..... 229 

,, liver in hepatic and portal thrombosis . . . . 148 

„ minute erosion (exulceratio simplex) of the gastric mucosa . . 73 

„ myoma of the oesophagus . . . . .73 

„ primary columnar-celled carcinoma of the tail of the pancreas . 171 

„ vacuolated carcinoma of the antrum .... 249 

RUSSELL (A. E.)> cysts of the pineal body . . .15 

,, and BUZZARD (E. P.), cysts in the liver containing living Para^ 

mcBcia colt ...... 149 

8AHTI (P. DE), central sarcoma of os calcis .... 198 
,, a case of multiple fibro-sarcomata of the scalp of nineteen years' duration ; 

removal of growths ; recurrence in the lungs . . . 234 

SHATTOCK (8. G.), an acromegalic skull and that of a normal giant . . 185 
,f chromocyte clumping in acute pneumonia and certain other diseases, 

and the signiflcance of the huffy coat in the shed blood . . 279 

„ enterolith from the rectum . . . . .134 

„ report of sub-committee on pseudo-tuberculosis . . 361 

STILL (Qt. P.), biliary calculi in children .... 151 
„ congenital hypertrophy of the pylorus . . . .86 

„ tubercular ulcer of the stomach in children . . .76 

THOMSON (H. C.)> & case of melanotic sarcoma with secondary growths of 

nnusual size in the small intestine .... 237 

VOELCKER (A. P.). an undescended left testicle . 183 

„ carcinoma of the cardiac end of the stomach . . 100 

WALSHAM (H.)> epithelial pearls in the tonsil . .65 

WARING (H. J.), adeno-lipoma of the submaxillary gland . . 67 

„ myeloid tumour of the neck ..... 232 

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INDEX 375 


WASHBOUBN (J. W.), discussion on pseudo-tubercnlosis . 344 

„ report of sub-committee on pseudo-tuberculosis 361 

WEBES (F. P.)> acute degeneration of liver cells supervening in the course 

of chronic cirrhosis. ..... 136 

„ an apparent thickening of subcutaneous veins .57 

„ contracted kidney with multiple adenomata . . .179 

„ diffuse syphilitic chauge in the liver .... 142 

yf small lipoma of kidney ..... IBl 

WETHESED (F. J.), discussion on pseudo-tuberculosis . 357 

WILS017 (T. S.), on dilatation of the right ventricle upwards and to the 

left . . . . . . .41 

WOODHEAD (0. S.), discussion on pseudo-tuberculosis ; introductory 

address . . . . . . .331 

„ report of sub-committee on pseudo-tuberculosis . . . 361 

WOODS-HUTCHUrSON^ discussion on pseudo-tuberculosis . 357 


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